The mechanism and kinetics of antianginal effect formation after laser therapy course in patients with angina pectoris

   Purpose: To assess some mechanisms of antianginal effect formation under low-level infrared laser irradiation in patients with angina pectoris, as well as to clarify the kinetics of this clinical effect after laser therapy course.

   Materials and methods. 88 male patients, aged 54.2 ± 3.7, with angina pectoris of functional class II–III were examined. 63 patients of the main group had a ten-day course of laser therapy. 25 patients were included in the control group in which laser irradiation was only simulated. At the initial stage and one month after laser therapy or its imitation, and in the main group additionally after 3 and 6 months, bicycle ergometric tests were performed to determine exercise tolerance and evaluate the double product indicator at the level of initial (P1) and maximum (P2) threshold load, if its threshold power exceeded the initial one.

   Results and discussion. The increase of exercise tolerance was observed in 79.5 % of patients from the main group one month later and in 81.7 % three months later after finishing laser therapy course, with the increase in exercise tolerance by 19.1 W (+ 30.4 %; p = 0.023) and by 22.7 W (36.2 %; p = 0.009), respectively. The antianginal effect lasted for about 6 months of follow-up in 62.0 % of treated patients. The double product indicator reflecting myocardial oxygen consumption at P1 level after laser irradiation had a pronounced downward trend. This indicator increased at maximum load (P2) by 19.1 % (p = 0.04) and by 24.1 % (p = 0.006) during repeated examinations in 1 and 3 months, respectively. By the sixth month of observation, studied parameters returned to the initial levels. There were no statistically significant changes in the studied parameters in patients from the control group.

   Conclusion. The data obtained indicate that a ten-day course of laser therapy triggers high and long-lasting antianginal effect in patients with angina pectoris. The mechanism of its action is caused with the economization factor of cardiac activity and with the increase of coronary blood flow productivity.

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