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Exercise Training for Refractory Angina: Why Does It Work?

These important findings are consistent with the physiology of exercise training and with the pathophysiology of ischemic heart disease. Total oxygen utilization during exercise is determined by cardiac output, equal to stroke volume times heart rate, multiplied by the amount of oxygen extracted from the blood [15] . In normal trained subjects, resting oxygen consumption can increase 13to 14-fold during maximum exercise, but only one third of this increase is due to changing cardiac output, which can increase about 4.5-fold (1.5fold for stroke volume and 3-fold for heart rate). The difference between changing oxygen utilization due to increased cardiac output alone and maximum oxygen availability during peak exercise is provided by an approximately 3-fold increase in arteriovenous oxygen (a-vO 2 ) difference across the working muscle beds of active people. Accordingly, much of the ability to exercise to a maximum level in normal subjects is a function of oxygen extraction, totally separate from any change in cardiac output [16] . What are the implications of these relationships for maximum exercise capacity in patients with stable refractory angina on maximal medication who are not suitable for further revascularization? In these patients, an increase in cardiac output during exercise may be constrained when stroke volume is limited by infarction or ischemia. Cardiac output may also be constrained when Cardiac rehabilitation with exercise training and ancillary support services remains one of the most effective treatments for heart disease [1, 2] . It can reduce mortality by 25–30% after myocardial infarction and improve survival after percutaneous coronary interventions [3– 5] . Exercise training can optimize physical capacity in chronic heart disease and after cardiac events, and perhaps more important, it can reduce cardiac work at the submaximal levels of activity that are reached during the general activities of daily living [6–9] . These outcomes favorably modulate symptoms of heart disease and restore confidence in physical capabilities for many patients. It is clear from data obtained prior to the routine use of percutaneous coronary interventions that patients with stable angina can benefit from exercise training [10– 13] . In this issue of Cardiology , Asbury et al. [14] present results from a pilot study of cardiac rehabilitation in patients with stable but refractory angina who have been maximally treated in the current therapeutic era and are not candidates for further revascularization. They show that cardiac rehabilitation in these patients can improve physical capacity as measured by walking time and distance without adverse effects on the frequency or severity of angina, and with concomitant improvement in psychological well-being and quality of life. Why does it work? Received: June 15, 2012 Accepted: June 19, 2012 Published online: July 27, 2012