Effects of cardiac disease on acquisition of heart rate control

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1978

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The majority of studies of voluntary self-control of heart rate have been conducted using college students as subjects. These studies have shown that self-control of heart rate is possible; that the extent of control is augmented by the provision of feedback; and that cardiac acceleration is more easily acquired than cardiac deceleration. Few researchers have studied the ability of persons other than young, healthy college students to alter their cardiac rate. Engel and his colleagues have utilized biofeedback training with patients suffering from cardiac disease, and have found that some were able to achieve a degree of cardiac control after a large number of training sessions. However, only Lang and his colleagues have systematically compared the response to brief cardiac biofeedback training of healthy young persons, healthy older persons, and older persons with heart disease. Lang found a hierarchical ordering of these groups in terms of their ability to decelerate their heart rate, with the healthy young subjects doing the best and the subjects with ischemic heart disease doing the poorest. The hierarchical ordering was not found for heart rate acceleration, however; both the older subjects with heart disease, and the healthy older subjects, proved unable to accelerate their cardiac rate significantly. The present study extended Lang's research by making a number of refinements in subject selection to achieve greater homogeneity of the patient group. Whereas Lang's patient group had in common only a history of ischemic heart disease, two heart disease groups were compared in the present research: patients who had suffered a first, uncomplicated myocardial infarction within the past month; and patients who had had one or more infarctions in the past, the most recent being no less than three months previously. No patients in the recent infarction group were taking cardiotropic drugs, and no patients in either the recent or past infarction group had had cardiac surgery. A control group of persons without known or detectable cardiac disease, matched in age to the two heart disease groups, was also studied. All subjects were given three brief biofeedback training sessions, one in cardiac acceleration and two in cardiac deceleration. Feedback was provided by a cardiotachometer, which reflected changes in heart rate on a beat-by-beat basis. The sessions included periods during which subjects were instructed to increase or decrease their heart rate without the feedback device being activated, as well as periods during which continuous feedback was provided. The results indicated that none of the three groups accelerated their heart rate significantly, either with or without feedback. This is consistent with Lang's findings, and may reflect the effects of increasing fibrosis of the heart with age. Significant heart rate deceleration was achieved by the control group, however, and the past infarction group's deceleration closely approached significance. The amount of deceleration was significantly greater when feedback was provided than when it was not. The recent infarction group was not able to decelerate their heart rate significantly, in spite of being just as responsive as the past infarction group to cardiac deceleration during an orienting task. Personality data indicated that anxiety was related to the ability to decelerate cardiac rate and that the control group was significantly less anxious than either of the two infarction groups. An explanation based upon the different effects of stress-aroused catecholamines on the scarred myocardium of the convalesced infarction patient and the irritable myocardium of the acute infarction patient was suggested; and possible motivational differences between these two groups were discussed.

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