Twenty male coronary heart disease (CHD) patients were divided into two groups at random qigong therapy group (mean age 62.6±1.63 years old) and placebo group (mean age 61.1±0.90 years old). The diagnosis of CHD was based on the history of typical angina pectoris and myocardial infarction combined with ECG findings and other laboratory analysis. Another 10 apparently healthy male subjects of similar age (51.7±1.16 years old) were studied as the control to compare with the laboratory findings.
Method:
In order to rule out the influence of the effects of movement, quiescent qigong exercise was selected. The exercise was similar to the relaxation qigong, and was done collectively in the morning. Then the patients did the exercise separately at least 2-3 times a day, lasting for about 30-45 min. each.
In the placebo group starch was used. The control healthy subjects did not enter any treatment program but the course of placebo was 2 to 3 months.
Measurement:
All of the subjects received the graded submaximal exercise test. Before and after the test, blood was drawn from both arms' antecubital vein with minimal occlusion. The blood samples were analyzed by radioimmunioassay to measure 6-K-P, the stable metabolite of prostacyclin (PGI2) and thromboxane B2 (TXB2) and the stable metabolite of thromboxane A2 (TXA2). Two weeks before experiment, all subjects had not taken any drugs known to interfere with the analysis of prostaglandins, such as aspirin, indomethacin, etc. The determination of plasma 6-K-P and TXB2 levels of all CHD patients were done again after a period of treatment.
Results:
1. Before the exercise, the plasma 6-K-P level and 6-K-P / TXB2 ratio of all CHD patients were significantly lower than those of healthy subjects (P<0.01). These agreed that atherosclerotic plague formation damaged the histologic and function integrity of the endothelium of the vessels in CHD patients, reduced production of PGI2 at the injured site,
causing the balance of PGI2-TXA2 to imbalance, and then made the condition from bad to worse. But the plasma TXB2 level didn't show any difference between CHD patients and the normal subjects. This might be explained by the different stage of diseases, most of the CHD patients in our experiment were chronic and stable ones.
2. Neither CHD patients nor healthy subjects had any changes of plasma 6-K-P, TXB2 and 6-K-P / TXB2 ratio after the submaximal exercise. Although we would not exclude the possibility of different response to different exercise and intensity, one conclusion could be drawn that submaximal exercise did not induce a PGI2-TXA2 imbalance in most chronic stable CHD patients.
3. Qigong training for one course significantly increased the plasma 6-K-P level (P <0.05) and 6-K-P / TXB2 ratio (P <0.0l), while in the placebo group, there was no alternation of these indices after the course, and so these values as compared with the qigong group, were significantly different. We suggested that during practice of the quiescent qigong exercise, the patients minds were in total concentration and the whole body should be highly relaxed, causing the patients to minimize the stress reaction. In the qigong state, the oxygen consumption was reduced, thus improving the oxygen supply to the tissues. In addition, the possible control and regulatory effects of qigong on the neuro humoral system and the ability of synthesis of PGI2 of the endothelium of vessel should be improved, then the imbalance of PGI2 -TxB2 in CHD patients could be ameliorated.
These findings confirmed the value of the qigong therapy in rehabilitation program for CHD patients.
