Origin of anterior descending branch of left coronary artery from pulmonary trunk.
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Biomedical subjects
Publications and source records attributed to M Niederberger.
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12 patients with the diagnosis of coronary heart disease and angina pectoris underwent evaluation of heart rate as an indicator of tolerance of a given work load. A floating catheter in a pulmonary artery and a peripheral arterial catheter permitted measurement of blood pressures. Oxygen uptake per minute (VO2) was measured by Douglas bags and oxygen content of arterial and mixed-venous blood was determined at rest and during each minute of submaximal and symptom-limited maximal exercise on a treadmill. In the minute of exercise, in which 60-80% (mean 71.3%) of maximal heart rate (HF max) were attained, VO2 averaged 60.3% VO2 max, cardiac output (Q) 72.5% Q max and mean pulmonary arterial pressure (PAP) 26.6 mm Hg. With one exception, Q leveled off or dropped in the last minutes of exercise beyond 85% HF max. Heart rate (HF), oxygen difference between arterial and mixed venous blood (DavO2) and PAP reached their highest values in the last minute. It is suggested that heart rates up to 70% HF max, as individually determined in a symptom-limited maximal exercise test, are the tolerable limit during occupational activities. 85% HF max should not be exceeded during exercise training. Left ventricular function may be impaired beyond that limit because of acute coronary or myocardial insufficiency, and the regulation of cardiac output becomes uneconomical.
Results of physical rehabilitation were studied in 2 groups of patients. Group A consisted of 16 men and at least 24 (mean 51.5) months had elapsed after myocardial infarction before they were entered into a training programme with supervised once-weekly classes in a school gymnasium. By contrast, the interval between infarction and onset of training was less than 12 (mean 7.0 months in the 21 patients of group B, who had exercise classes twice a week. Group A achieved an average increase in estimated aerobic capacity of 32% (p less than 0.001) in 10 months of training, group B of 33% (p less than 0.001) in 4.7 months. Further participation of group A for 26 more months resulted in an additional improvement of 11% (p less than 0.05). Differences between the groups in aerobic power and different methods of exercise testing and training are discussed. The results indicate that early physical training of groups of patients helps them to obtain a normal exercise capacity with a year after myocardial fixation. Without such intervention patients often remain restricted, but with supervised training their physical power may be improved significantly even if years have passed after the heart attack.
9 patients with diagnosis of coronary heart disease (CHD) and typical angina pectoris (AP) were studied by means of a multistage, symptom-limited treadmill test and a similar bicycle ergometer (bike)-test. The sequence of tests was determined by chance. Between the tests, the patients rested one hour. Oxygen uptake (vo2) was determined by the Douglas-bag-method, blood pressures were measured via catheters placed in a pulmonary and a brachial or radial artery, respectively. Cardiac output (Q) was calculated by the direct Fick principle. In all tests, with the exception of one bike-test, all patients were limited by AP. They attained high VO2 (mean 1316 ml/min) on the treadmill (TM) while on the TM their mean arterial blood pressure (BP) was significantly (P greater than 0.05), namely 10 mm Hg as an average, lower. Comparing the final minute -3 of the TM-test with the final minute -1 of the bike-test in 5 patients, we found heart rate (HR), BP and pressure rate product (HR times BP) lower on the TM (P greater than 0.05), whereas VO2 was the same. Patients, whose exercise performance is limited by angina pectoris on bike and TM, achieve higher VO2 on the treadmill, together with lower BP. This may be of clinical importance in exercise-testing and -training of patients with CHD.
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