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Atrial fibrillation is associated with an increased risk of stroke. Different risk factors may be of importance regarding stroke incidence and mortality in atrial fibrillation. Retrospectively, we studied 786 patients with chronic atrial fibrillation, 229 with rheumatic heart disease and 557 without. In all, 127 patients had stroke (16%). Using Cox's proportional hazard model for failure-time data with age, gender, etiology, degree of heart failure and cardiac enlargement as explanatory (independent) variables, only etiology (rheumatic heart disease) was a significant risk factor for stroke (P<0.006). Significant risk factors for death in 653 patients without stroke were age (P= 0.000) and congestive heart failure at the onset of atrial fibrillation (P = 0.000). The need to identify other risk factors for stroke in patients with atrial fibrillation is emphasized, for selecting patients at high risk for prophylactic treatment with anticoagulants or aspirin. [ABSTRACT FROM PUBLISHER]

The effect of exercise upon right and left ventricular ejection fractions (RVEF and LVEF) as well as the changes upon left ventricular end-diastolic and end-systolic volume indices (LVEDVI and LVESVI) were investigated. Twenty-two normal subjects were studied at rest and during upright submaximal exercise. RVEF was determined using a first-pass method. LVEF was measured using multiple gated blood pool imaging. During the exercise test ECGs remained normal. HR and BP increased significantly (P<0.01). RVEF increased from 44%±4 (mean±SD) to 60%±6 (P<0.001). LVEF increased from 62%±6 to 76±5 (P<0.001). A wider scatter was observed in ΔRVEF than in ΔLVEF. There was a 14% increase in LVEDV-index and a 14% decrease in LVESV-index (P<0.001). A multiple regression analysis with ΔRVEF as the dependent variable and ΔHR, Δsystolic BP, ΔLVEF, ΔLVEDV-index and LVESV-index as independent variables showed a significant correlation between ΔRVEF and ΔLVEF and δsystolic BP (P<0.05). Our data provide insight into the mechanisms by which the pump performance is increased in normal subjects. The central mechanisms observed are the Starling effect and an increase in contractility of the myocardium. This is connected in the general circulation to an increase in afterload, indicating a redistribution of blood from the vascular beds to the muscles and to the heart. [ABSTRACT FROM PUBLISHER]

Eight healthy people (seven men and one woman, aged 19 to 31 years) were studied by radionuclide cardiography when supine before and 30 minutes after a standard meal (6300 kJ). Control investigations were performed on a different day within a week of the standard meal. There was a median increase in cardiac output of 62% that was attributable to a 17% increase in heart rate and a 41% increase in stroke volume. Blood pressure and concentrations of plasma catecholamines did not change. The median end diastolic and end systolic volumes of the left ventricle increased by 41% so that the left ventricular ejection fraction was unchanged. There were no significant changes during the control experiments. In healthy people a meal caused an appreciable increase in stroke volume and dilatation of the left ventricle. The activity of the sympathetic nervous system, as measured by plasma catecholamines, did not change much, and changes in blood volume alone did not seem to explain the haemodynamic response to the meal. [ABSTRACT FROM PUBLISHER]

A statistical model based on the method of variance components was applied to obtain confidence statements for single and repeat determinations of left ventricular ejection fraction by radionuclide techniques. With this approach variance caused by individual factors in the measurement procedure is estimated to allow calculation of confidence intervals based on single measurements and the detection limits for changes. Six study groups made up of a total of 143 subjects were examined by both multigated equilibrium and first pass imaging. Under favourable conditions (with an updated gamma camera and experienced observer) the 95% confidence interval with a single measurement of left ventricular ejection fraction by equilibrium imaging was +/- 3 ejection fraction units, compared with +/- 6 units with the first pass technique (one ejection fraction unit = 1/100 of the possible values from 0.00 to 1.00). The minimal significant changes (at the 5% level) in measured equilibrium left ventricular ejection fraction at intervals of 15 min, 3 days, 1, 3, and 4 weeks were +/- 4, +/- 4, +/- 5, +/- 5, and +/- 6 units, respectively. The corresponding minimal detectable changes in a subject's "true" left ventricular ejection fraction for the same intervals were +/- 7, +/- 7, +/- 10, +/- 10, and +/- 12 units respectively. With first pass imaging, only average values for the variation at repeat determination could be calculated. The minimal significant change in measured first pass left ventricular ejection fraction was +/- 7 units, and the minimal detectable change in "true" left ventricular ejection fraction was +/- 14 units. Measurements of left ventricular ejection fraction by equilibrium technique were generally more reproducible than first pass determinations because the variability caused by study acquisition, observer analysis, and residual errors was smaller. The method of variance components appears to be well suited to the evaluation of quantitative biological measurements in clinical use. The popularity of established procedures may obscure the lack of basic information about method evaluation. [ABSTRACT FROM PUBLISHER]

Left ventricular performance was studied non-invasively in 24 chronic alcoholics without liver disease. Twelve patients who had abstained from drinking for at least one month (group A) and 12 sex and age matched patients who had ceased drinking during the preceding 24 hours (group B) were studied at rest and during 50% submaximal exercise. Cardiac output and stroke volume were measured by first passage and left ventricular ejection fraction by multigated radionuclide cardiography. Twelve healthy sex and age matched controls were also studied. Haemodynamic variables were similar in group A and the controls, except that in group A left ventricular end systolic volume index did not decrease during exercise. In group B the heart rate was increased both at rest and during exercise and plasma noradrenaline concentrations were increased. The stroke volume index did not increase significantly during exercise in group B. In addition, the increase in left ventricular ejection fraction was smaller in group B than in controls. End systolic contraction was reduced in group B patients and diastolic blood pressure was increased. These results suggest that cardiac abnormalities in chronic alcoholics may be reversed after cessation of drinking if no chronic liver disease is present. Recent alcohol consumption increases sympathetic nervous activity, impairs cardiac contractility, and increases afterload during physical stress. [ABSTRACT FROM PUBLISHER]