Exercise has been advocated for the treatment of intermittent claudication for nearly half a century. During this time, exercise rehabilitation has been shown to improve walking ability, performance, and energy efficiency on graded treadmill testing, as well as improve other measures of ambulatory walking ability. 1,2 There is an improvement with exercise in functional capacity with an increase in maximal oxygen consumption. 1 Furthermore, there are improvements in the perceived walking ability by patients in the community setting. Importantly, this has translated into improved physical activity with greater free-living daily activity. 2 To achieve maximal benefit, the components of exercise programs include a program of at least 6 months duration with at least three exercise sessions per week, each lasting at least 30 minutes. 3 The mode of exercise should be walking with exertion to the point of near-maximal pain onset. In this issue of the Journal of Cardiopulmonary Rehabilitation, the study by Gardner and colleagues 4 confirms many of the earlier findings while extending the benefit of exercise beyond the initial 6-month program into a 12-month maintenance phase. Although there are limitations to this study-including the small size and subject attrition, especially in the control group, leading to potential bias-this was a randomized trial that used well-established, objective methodologies. These findings are important if the effects of an exercise program are intended to alter the life of those with peripheral arterial disease in the long-term.
Survival is impaired in those with peripheral arterial disease, comparable to those with coronary artery disease, with a 5-year mortality rate of 30%. This increased mortality is attributed to the greater prevalence of coexistent coronary artery disease in those with peripheral arterial disease. It appears, however, that the risk extends beyond that attributed simply to the presence of coronary artery disease. It has been shown that in people with multi-vessel coronary disease, despite similar coronary anatomy and ventricular function, the presence of peripheral arterial disease greatly impairs survival, with a nearly fivefold increase in the relative risk. 5 The cause of this increased risk is unclear, but it is likely that impaired functional capacity and reduced physical activity are key factors. It is known that those with peripheral arterial disease have a reduced functional capacity by approximately 50% compared to a healthy population-similar to that observed with advanced heart failure. 1 This reduced physical capacity leads to reduced physical activity during the day, which may contribute to the increased mortality. In contrast, there appears to be a reduction in the risk of mortality as physical activity increases in both healthy adults and those with cardiovascular disease. 6,7
There is a great potential for exercise rehabilitation in intermittent claudication to modify the cardiovascular risk. It has been shown previously that exercise rehabilitation is associated with an improvement in various parameters, including blood pressure and lipid profile, in patients with peripheral arterial disease. 8 Although the significance is unclear, there also is an improvement in endothelial function and nitric oxide-mediated dilation, supporting favorable affects on the vascular milieu that may inhibit subsequent thrombotic events. 9 It appears that the improvement in functional capacity and walking ability translates into increased free-living daily activity with greater caloric expenditure. 4 These changes in physical activity may modify the risk of future cardiac events. As previously emphasized, inactive or sedentary individuals with coronary artery disease who become at least lightly active have a reduced risk relative compared with those who remain inactive (relative risk 0.58, 95% confidence interval 0.33-1.03;P = .006). 7
Despite the clear benefits of exercise in the treatment of intermittent claudication, access to supervised (or partially supervised) exercise programs often is limited. A major impediment to participation has been a lack of reimbursement for such programs by third-party payers. This is in contrast to the more readily available programs for cardiac rehabilitation, in large part as a result of the availability of such reimbursement. No studies have been performed to show a benefit of vascular rehabilitation in reducing cardiovascular events. However, given the potential value to the healthcare system, extrapolation of the benefits achieved in cardiovascular rehabilitation to those anticipated with exercise therapy for intermittent claudication seems reasonable. After acute myocardial infarction, cardiovascular rehabilitation has been shown to reduce mortality in a meta-analysis of several randomized controlled trials. 10 The pooled odds ratio of 0.76 for all-cause death in the rehabilitation group was significantly lower than in the control group.
To achieve long-term lifestyle changes in physical activity, the benefits of exercise rehabilitation would need to be sustained. It is well known that the clinical benefits and improvement in functionality obtained with exercise rehabilitation in intermittent claudication rapidly dissipate after exercise is stopped. The article by Gardner and colleagues demonstrated the continued benefit of exercise for intermittent claudication after transitioning to a maintenance program of long duration. This persistent benefit is essential if such programs are to sustain life modifying and potentially life prolonging effects. It appears possible that long-term exercise, by maintaining the initial improvement in functional status and peripheral circulation, may reduce ischemic-related cardiovascular complications. Although untested, preliminary work and extrapolation of the benefits of cardiovascular rehabilitation provides support for this possibility.
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