Clinical factors associated with delay time in suspected acute myocardial infarction.
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Adult↗
Biomedical subjects
A Hjalmarson
Publications and source records attributed to A Hjalmarson.
The prognosis of patients suspected of having acute myocardial infarction subsequent to its exclusion as the diagnosis.
This review of the literature concerns the prognosis of patients suspected of having myocardial infarction subsequent to its exclusion as the diagnosis. Several investigations show a surprisingly bad prognosis for patients in this category, almost comparable to that of patients with a confirmed infarction. When the results of the different studies are pooled, however, there is a significant difference between those patients with true infarction, and those in whom infarction was excluded, in terms of overall mortality (12% and 7%; P less than 0.0001) and the development of subsequent non-fatal infarction (11% and 6%; P less than 0.05) when the results are analysed for a period of follow-up of one year. The difference was significant even when both fatal and non-fatal infarctions were taken into account over the one-year period of follow-up (13% and 8%; P less than 0.0001). The analysis shows that electrocardiographic ST-T changes are a risk factor for coronary events, but the results are conflicting for other possible risk factors. The selection of patients varies between the different studies, which probably contributes to the different results reported. Prospective studies with well defined groups of patients large enough to permit analysis of subgroupings will be needed to resolve the outstanding questions.
Diagnostic Errors↗
A new insight into adriamycin-induced cardiotoxicity.
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Cardiolipins↗
Mortality and morbidity during one year of follow-up in suspected acute myocardial infarction in relation to early diagnosis: experiences from the MIAMI trial.
From a large randomized multicentre trial of metoprolol in suspected acute myocardial infarction (n = 5778) we report on the outcome during 1 year of follow-up, in relation to early diagnosis. Patients who developed a confirmed infarction had a 1-year mortality rate of 12.8%. This was significantly higher than the mortality rate of 6.3% (P less than 0.001) in patients with possible infarction and it was also higher than that in patients with no infarction, which was 5.0% (P less than 0.001). A multivariate analysis showed that independent risk predictors in the clinical history of patients without confirmed infarction were a history of angina pectoris, chronic use of digitalis and advanced age. After 1 year, angina pectoris was most common in patients with an initial possible infarction. These patients were also in most urgent need of bypass surgery. We thus conclude that the mortality during 1 year of follow-up among patients with an initially strongly suspected acute myocardial infarction was clearly related to whether or not the patient developed a myocardial infarction.
Angina Pectoris↗
Eligibility for intravenous thrombolysis in suspected acute myocardial infarction.
Based on the registration of all the 7,157 patients admitted during a 21-month period to the emergency ward of a single hospital in an urban area with chest pain or other symptoms suggestive of acute myocardial infarction, we studied eligibility for intravenous thrombolysis in suspected acute myocardial infarction. We have limited the present analysis to those 1,715 patients with a strong suspicion of myocardial infarction, and for these patients, we have calculated the percentages eligible for thrombolysis when various electrocardiographic and delay time criteria are applied, but we have not considered contraindications to thrombolysis. We have also calculated the proportions of all infarctions in this group that would thereby receive the treatment, and the proportions of patients treated that would develop a confirmed infarction. Using the criteria ST elevation on the initial electrocardiogram and arrival in hospital within 6 hours from onset of symptoms, 18% of patients would have been given early intravenous thrombolysis, 37% of confirmed infarctions would have been treated, and 91% of all treated patients would have developed a confirmed infarction; with a delay time criterion of 12 hours, these percentages would have been 20%, 41%, and 91%, respectively; with a criterion of 24 hours, they would have been 22%, 45%, and 90%, respectively. By not considering the initial electrocardiogram and applying only the criterion of delay time, these percentages would have been 70%, 72%, and 45%, respectively, for a delay time of 6 hours; 83%, 84%, and 45%, respectively, for a delay time of 12 hours; and 91%, 92%, and 44%, respectively, for a delay time of 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
Electrocardiography↗
Mapping of a functional autoimmune epitope on the beta 1-adrenergic receptor in patients with idiopathic dilated cardiomyopathy.
The presence and properties of serum autoantibodies against beta-adrenergic receptors in patients with idiopathic dilated cardiomyopathy were studied using synthetic peptides derived from the predicted sequences of the human beta-adrenergic receptors. Peptides corresponding to the sequences of the second extracellular loop of the human beta 1- and beta 2-adrenergic receptors were used as antigens in an enzyme immunoassay to screen sera from patients with dilated cardiomyopathy (n = 42), ischemic heart disease (n = 17), or healthy blood donors (n = 34). The sera of thirteen dilated cardiomyopathy patients, none of the ischemic heart disease patients, and four of the healthy controls monospecifically recognized the beta 1-peptide. Only affinity-purified antibodies of these patients had a inhibitory effect on radioligand binding to the beta 1 receptor of C6 rat glioma cells. They recognized the receptor protein by immunoblot and bound in situ to human myocardial tissue. We conclude that a subgroup of patients with idiopathic dilated cardiomyopathy have in their sera autoantibodies specifically directed against the second extracellular loop of the beta 1-adrenergic receptor. These antibodies could serve as a marker of an autoimmune response with physiological and/or pathological implications.
Adult↗
Early use of metoprolol and serum potassium in suspected acute myocardial infarction.
In 1350 patients with suspected acute myocardial infarction, serum potassium was analysed in the emergency ward. The effect of metoprolol was compared with placebo in a double-blind randomized trial. Metoprolol increased serum potassium from 4.11 +/- 0.02 mmol/l to 4.27 +/- 0.02 mmol/l (P less than 0.001) during the 1st day after hospital admission, whereas serum potassium levels remained fairly constant in patients given placebo during the same time (4.11 +/- 0.02 to 4.14 +/- 0.02 mmol/l; P greater than 0.2). Similar results were obtained when analysing patients with a confirmed myocardial infarction separately. The effects appeared homogeneously distributed in subgroups related to sex, clinical history, infarct site, infarct size and delay time from onset of symptoms to start of treatment. We conclude that early treatment with the beta-1-selective blocker metoprolol in patients with suspected acute myocardial infarction increases serum potassium.
Clinical Trials as Topic↗
Effects of metoprolol on mortality and late infarction in diabetics with suspected acute myocardial infarction. Retrospective data from two large studies.
From two large scale studies in patients with suspected acute myocardial infarction we report the outcome in diabetics after treatment with either metoprolol or placebo. In the Göteborg Metoprolol Trial mortality at 3 months was reduced by metoprolol from 17.9% to 7.5% and late infarction was reduced from 16.4% to 3.8%. In the MIAMI Trial, mortality was decreased by metoprolol from 11.3% to 5.7% and the occurrence of late infarction was decreased from 4.5% to 3.1% during 15-day follow-up. Compared with the overall results, the effect of metoprolol on mortality appears particularly impressive in diabetics.
Diabetes Complications↗
Quality of life five years after myocardial infarction.
In 539 patients 5 years after myocardial infarction (MI), quality of life and factors influencing life quality were studied. All patients originally participated in an early intervention trial with metoprolol. A cardiac follow-up questionnaire and the Nottingham Health Profile were answered by 82%. In the former, information about subjective symptoms, smoking, work and current medication was obtained; the latter described health-related quality of life in terms of energy, sleep, emotions, mobility, pain and social isolation. The rate of and the reasons for rehospitalization were registered in the patients' records. The MI patients reported a comparatively high quality of life. Compared with 'normal' population, a decrease was noted in energy, sleep and mobility, and in sex life, hobby-activity and holiday activity. A nonparametric multivariate analysis disclosed that dyspnoea, angina pectoris and anxiety were closely associated with decreased quality of life. In conclusion, 5 years after MI most patients seemed well-adjusted. Impaired quality of life was reported by patients suffering from angina pectoris, dyspnoea and emotional distress. No relationship was found between health-related quality of life and the beta blocker, metoprolol, which was the most frequently used drug.
Angina Pectoris↗
Treatment of pain in acute myocardial infarction.
The treatment of pain in acute myocardial infarction varies with local practice. Narcotic analgesics are still the usual treatment in many hospitals. Knowledge of optimal doses, duration of pain relief, and time between drug administration and pain relief is inadequate. Many studies indicate that the relief of pain is often incomplete after treatment with narcotic analgesics. There is often a need for alternative treatments. Large randomised studies consistently show that beta blockade, initially given intravenously and then orally, relieves pain and reduces the need for analgesics. Studies also indicate that early administration of streptokinase and glyceryl trinitrate relieves pain. There is evidence that drugs that limit ischaemic damage also relieve pain.
Adrenergic beta-Antagonists↗
Short- and long-term clinical outcome after Q wave and non-Q wave myocardial infarction in a large patient population.
Prognosis for patients with non-Q wave myocardial infarction is controversial although a number of studies have shown a less favorable outlook after hospital discharge for patients with non-Q wave than for those with Q wave infarction. Therefore, the in-hospital and 1-year prognosis was investigated in a sufficiently large patient population (n = 2,024) to allow stratification by subgroups, in particular by age and previous myocardial infarction. Patients with non-Q wave infarction (n = 444; 22% of the total study population) were somewhat older (65 vs. 63 years, p less than 0.001) and had an increased incidence of previous myocardial infarction (46% vs. 24%, p less than 0.001) and congestive heart failure (21% vs. 8%, p less than 0.001) than patients with Q wave infarction. In-hospital mortality of patients with non-Q wave infarction was lower (8.1% vs. 11.5%; p less than 0.06), whereas their 1-year mortality after hospital discharge was significantly higher (13.7% vs. 9.2%, p less than 0.05) than for patients with Q wave infarction. However, total mortalities at 1 year were nearly equal. When patients were subgrouped by presence or absence of a previous myocardial infarction, patients in both subgroups exhibited mortality patterns typical of the entire population with Q wave or non-Q wave infarction. However, when stratified by age and previous infarction, in-hospital mortality for patients with non-Q wave infarction was significantly lower only in patients older than 70 years of age. Similarly, the higher mortality after hospital discharge in patients with non-Q wave infarction occurred only in patients older than 70 years of age without previous myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
Age Factors↗
Differing circadian patterns of symptom onset in subgroups of patients with acute myocardial infarction.
Circadian variation of the onset of acute myocardial infarction has been noted in many studies and may carry important pathophysiologic implications. However, only a few previous studies have attempted subgroup analyses. In 4,796 patients with documented acute myocardial infarction, the time of symptom onset was recorded. As in other studies, the peak of onset occurred in the morning from 6:01 AM to 12:00 noon, and 28% of the population (1.16 times the average percentage for the other time periods) experienced symptom onset in that period (p less than 0.001). There was a second, lower peak (25%) in the evening between 6:01 PM and 12:00 midnight, which was also observed in some previous studies. We sought to determine whether or not the presence of subgroups with specific clinical characteristics would exhibit different patterns and thereby contribute to these peaks in the overall population. In patients with a history of congestive heart failure (n = 606) or with non-Q wave infarction (n = 832), a pronounced peak (29%) occurred only in the evening. Two nearly equal peaks were observed in patients older than 70 years of age (n = 1,422), smokers (n = 2,057), diabetics (n = 767), women (n = 1,213), and patients taking beta-blocking drugs (n = 847). Finally, in patients with a previous myocardial infarction (n = 1,104), no peaks were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic beta-Antagonists↗
Long-term beta-blockade in dilated cardiomyopathy. Effects of short- and long-term metoprolol treatment followed by withdrawal and readministration of metoprolol.
To evaluate the short- and long-term effects of beta-adrenergic blockade (metoprolol) as well as the reaction to withdrawal and readministration of metoprolol in severe heart failure, 33 patients (25 men and eight women; mean age, 47.6 +/- 14.0 years) with dilated cardiomyopathy were studied by right and left heart catheterization, right ventricular biopsy, two-dimensional and Doppler echocardiography, and external pulse recordings. Twenty-six of 33 patients survived more than 6 months, and 24 of the 26 patients improved their functional class (from mean 3.3 to 1.8, p less than 0.0001). These 24 patients were subjected to withdrawal of metoprolol until the number of symptoms increased and deterioration occurred as observed noninvasively (group 1, n = 16), whereas the eight patients did not deteriorate during a 12-month period (group 2). During long-term treatment with metoprolol, there was an increase in ejection fraction from 0.24 to 0.42 (p less than 0.0001), whereas there was a decrease in the left ventricular (LV) end-diastolic dimension (from 7.3 to 6.4 cm, p less than 0.0001), in the grade of mitral regurgitation (from 1.7 to 0.4, p less than 0.0001), and in the grade of tricuspid regurgitation (from 0.6 to 0.05, p less than 0.007). There was a decrease in pulmonary wedge pressure (from 23.8 to 10.7 mm Hg, p less than 0.0001), LV end-diastolic pressure (from 24.1 to 13.4 mm Hg, p less than 0.002), and systolic vascular resistance (from 1,782 to 1,499 dynes/sec/cm, p less than 0.04). There was an increase in systolic blood pressure (from 116 to 132 mm Hg, p less than 0.003), cardiac index (from 2.17 to 2.58 l/min/m2, p less than 0.005), and LV stroke work index (from 31 to 65 g.m/m2, p less than 0.0001). During withdrawal of metoprolol, the heart rate and left atrial dimension increased (p less than 0.0001), whereas ejection fraction decreased (p less than 0.0001). The 12 (of 16) patients in group 1 who survived the withdrawal period had metoprolol readministered, and subsequently, ejection fraction increased (from 0.23 to 0.33, p less than 0.002). Patients had a low number of ventricular beta-adrenergic receptors compared with healthy control subjects (30.3 +/- 2.9 vs. 97.4 +/- 8.7 fmol/mg protein, p less than 0.001), but long-term treatment with metoprolol caused a moderate up-regulation (from 30.3 +/- 2.9 to 49.0 +/- 7.1 fmol/mg protein, p less than 0.05), which may facilitate a more normal response to sympathetic stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)
Adolescent↗
Effects of malnutrition on rat myocardial beta-adrenergic and muscarinic receptors.
Malnutrition, as well as malignancy, induces alterations in heart metabolism and performance. Previous studies have implicated adrenergic mechanisms as the cause. The present study was undertaken to investigate if the adenylate cyclase system in the rat heart was affected by malnutrition. Three different animal groups with malnutrition were compared with a control group: rats with acute starvation for 14-96 hours, rats with protein-calorie malnutrition for 2 weeks, and rats with tumors. Stimulation by beta-adrenergic receptors and inhibition by muscarinic receptors of adenylate cyclase activity were not altered by malnutrition. However, conditions used for in vitro adenylate cyclase determinations were, of necessity, not physiological. Neither did the number of beta-adrenergic and muscarinic receptors change. When competition-binding experiments were performed, differences comprising agonist affinity and affinity state distribution were noted among the groups. The myocardial beta-adrenergic receptors formed a reduced number of high-affinity sites in all groups as compared with the control rats. All high-affinity sites displayed a more than 10-fold increase in affinity toward isoproterenol and an impaired sensitivity to guanine nucleotides except in heart membranes derived from rats starved less than 48 hours. While the protein-calorie restricted and the tumor-bearing rats had myocardial beta-adrenergic receptors that were unresponsive to guanine nucleotides, after 48 hours of starvation the rats exhibited an attenuated guanine-nucleotide-induced affinity shift. No changes associated with malnutrition in myocardial membrane levels of the of the stimulatory guanine-nucleotide-binding protein were detected by cholera-toxin-induced ADP-ribosylation.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenylyl Cyclases↗
Quality of life in postmyocardial infarction patients in relation to drug therapy.
Quality of life (QL) was assessed in relation to drug therapy in 539 patients who were still alive five years after myocardial infarction (MI), and the interaction between drug therapy and QL was investigated. The patients originally participated in a double-blind trial that evaluated the effect of early administration of the beta blocker metoprolol. A cardiac follow-up questionnaire (CFQ) and the Nottingham Health Profile (NHP) were answered by 82%. In the CFQ, sel-fassessed cardiac symptoms, medication (diuretics, digitalis, antiarrhythmics, long-acting nitrates, beta blockers, psychoactive drugs), smoking habits, and work status were described. NHP described QL within the sections of mobility, energy, pain, sleep, emotional reactions, and social isolation. The independent relation between morbidity, drugs, and QL was analyzed multivariately. Apart from symptoms of angina pectoris and dyspnoea, anxiety resulted in impaired QL. A relation between diuretics and decreased QL was found, but no indications of adverse effects of the beta blocker metoprolol.
Anxiety↗
Antigenic analysis of the second extra-cellular loop of the human beta-adrenergic receptors.
Polyclonal antibodies were raised in rabbits by immunization with free peptides corresponding to positions 197-222 of the human beta 1-adrenergic receptor (beta 1 peptide) and the corresponding sequence (172-197) of the human beta 2-adrenergic receptor (beta 2 peptide). While the beta 2 peptide yielded antibodies that cross-reacted with the beta 1 peptide, the antibodies against the beta 1 peptide did not cross-react with the beta 2 sequence. Cross-reactivity of the anti-beta 2 peptide antibodies and the selectivity of the anti-beta 1 peptide antibodies were also revealed in the recognition by immunoblots of the beta 1- and beta 2-adrenergic receptors of different species or of the receptor gene products expressed in a bacterial vector. These antibodies could be used immunohistochemically to visualize the beta-adrenergic receptors on rabbit heart. The anti-beta 2 peptide antibodies did not show any functional effect on the beta-adrenergic receptors; the anti-beta 1 peptide antibodies were able to displace agonist affinity to higher values. Recognition of truncated peptides by the anti-beta 1 and anti-beta 2 peptide antibodies suggested that the cross-reaction of the anti-beta 2 peptide antibodies was due to the recognition of a common epitope on the C-terminal part of the peptides. The anti-beta 1 peptide antibodies recognized the N-terminal part of the peptide better than the C-terminal part. These results suggest that the second extracellular loop postulated in the structure of the human beta-adrenergic receptor contains the T and B cell epitopes necessary for induction of an immune response. The selectivity and the functional properties of the antibodies raised against that loop in the beta 1 adrenergic receptor could have relevance in induction of auto antibodies in certain cardiomyopathic conditions.
Antibodies↗
Identification of the interstellar cyanomethyl radical (CH2CN) in the molecular clouds TMC-1 and Sagittarius B2.
We report the astronomical identification of the cyanomethyl radical, CH2CN, the heaviest nonlinear molecular radical to be identified in interstellar clouds. The complex fine and hyperfine structures of the lowest rotational transitions at about 20.12 and 40.24 GHz are resolved in TMC-1, where the abundance appears to be about 5 x 10(-9) relative to that of H2. This is significantly greater than the observed abundance of CH3CN (methyl cyanide) in TMC-1. In Sgr B2 the hyperfine structure is blended in the higher frequency transitions at 40, 80, and 100 GHz, although the spin-rotation doubling is clearly evident. Preliminary searches in other sources indicate that the distribution of CH2CN is similar to that for such carbon chain species as HC3N or C4H.
Acetonitriles↗
[Beta blockade after myocardial infarction or not?].
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Adrenergic beta-Antagonists↗