[Cardiac volume and work capacity in young athletes as dependent on the direction of the training process].
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Oxidative stress stimulates both growth and apoptosis in cardiac myocytes in vitro. We investigated the role of oxidative stress in the initial phases of cardiac remodeling induced in an animal model by volume overload. As plausible candidates for a connection between oxidative stress and cardiomyocyte apoptosis or hypertrophy, we explored the behaviour of two MAPKs, specifically JNK and ERK. At 48 h of overload, the greatest increase in oxidative stress coincided with a peak of cardiomyocyte apoptosis. This was possibly induced through the mitochondrial metabolism, as evidenced by the release of cytochrome c and a significant increase in the active forms of caspase-9 and -3, but not caspase-8. Oxidative stress markers significantly decreased at 96 h of overload, combined with a marked attenuation of apoptosis and the appearance of hypertrophy. The highest levels of JNK and the lowest levels of ERK phosphorylation were observed at 48 h of overload. Conversely, a sharp increase in ERK phosphorylation was detected at 96 h of overload coinciding with the hypertrophic response. Together these results show that oxidative stress is an early and transient event in myocardial volume overload. They suggest that oxidative stress mediates amplitude dependent apoptotic and hypertrophic responses in cardiomyocytes through the selective activation of, respectively, JNK and ERK.
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A radiographic and hemodynamic investigation has been performed in 53 patients with pure isolated aortic regurgitation, in order to evaluate the most reliable method to detect left ventricular enlargement in this condition. Twelve plain chest film measurements have been compared to the end diastolic volume of the left ventricle calculated by left ventricular angiography. The most sensitive detector of left ventricular enlargement was the plain film total heart volume ( r = 0.754); the cardiothoracic ratio, the cardiac perimeter and the frontal area were less sensitive measurements, but still statistically significant (p less than 0.001). The results of our investigation support the conclusion that plain film total heart volume is the most reliable single measurement for evaluating the left ventricular enlargement in patients with isolated pure aortic incompetence.
Myocardial stereo-microangiography was performed on 30 rats after swimming exercise for one or two periods with and without a previous operation for production of aortic stenosis. In 8 rats with aortic stenosis no swimming exercise followed, and 10 more rats served as normal controls. Swimming exercise resulted in a higher degree of cardiac hypertrophy than aortic stenosis. Both types of cardiac hypertrophy resulted in vascular adaptive reactions in the myocardium. The adaptive reaction to swimming exercise was found to be persistent, at least to some extent, and to be of use if the exercise was resumed. The adaptive alterations in aortic stenosis were further modified by a superimposed period of exercise, although the nutritive capillary vasculature only showed a slight and focal increase in density.
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An improved isotope method for direct and non-invasive determination of heart volume, ejection volume and volume/time is described. By taking account of the reduction in the radio-active marker during the procedure, very good correlation of the results with those of cine ventriculography carried out at the same time can be expected.
Examination of 32 patients with aortic stenosis permitted the author to establish quantitative relationships between the dimensions of the left atrium and the continuous form of atrial fibrillation, between the dimensions of the left atrium, the heart volume and paroxysmal atrial fibrillation. Atrial fibrillation develops in aortic stenosis in the terminal stage of the disease. Quantitative relationships between the dimensions of the left atrium and continuous atrial fibrillation are similar to those in mitral incomperence which is evidence by the similarity of hemodynamic disorders in the left atrium in mitralism during aortic stenosis and mitral insufficiency.
Volumetric image display and analysis techniques have been under development to support x-ray computed tomographic (CT) imaging of the heart and lungs since the mid 1970s when investigators began to understand the image analysis requirements for the Dynamic Spatial Reconstructor. With the spread of Imatron's C-100 scanners (Imatron, South San Francisco, CA) around the world along with the development of slower helical scanners that generate volumetric information, there is an increased interest in the use of volume visualization and analysis tools to study the cardiopulmonary system. An historic overview of the development of such volume visualization for x-ray CT scanning is given along with a discussion of techniques for data acquisition, volumetric display, and image quantitation. We further show throughout the discussion how the integration of tools into a comprehensive image display and analysis software package (the tool box) enhances the utility of the individual tools. An example of such a tool box is given in a discussion of an X Windows-based package dubbed VIDA.
All males of the district Cottbus who suffered from an acute myocardial infarction between 1 June 1973 and 30 June 1974 and survived the first rehabilitation phase of a definite myocardial infarction were included in the study. Their arterial lactate level, the oxygen intake, the heart rate and heart size were determined by means of standardized ergometry and radiology. Patients who had performed a rehabilitation training programme showed a higher efficiency and equal values of lactate level and heart rate compared with the patients without training programme. A close correlation also existed between lactate level and heart rate. There was no dependence on the age of the patient or the degree of heart insufficiency. These results allow to conclude that the lactate level can be used for the determination of the training intensity of patients after an acute myocardial infarction.