Number 16
PNEUMATIC LIMB COMPRESSION: A FREE LUNCH? INVITED COMMENTS
John M. Porter, MD. Division of Vascular Surgery, Oregon Health Sciences University, Portland, OR
J Vasc Surg 2000;31:821-2
As the old adage reminds us, beware of something too good to be true: it probably is. The notion of obtaining permanent circulatory benefits in an ischemic limb by temporary intermittent pneumatic compression has been hovering around the edges of vascular practice for decades. The concept reemerged in recent years and now has a patina of scientific respectability by the article by Delis and associates in this issue of the Journal of Vascular Surgery.
I have historically dismissed this concept as non-sense: A quest for a perpetual motion machine, in fact, a free lunch. Long experience has taught that one rarely gets something for nothing, and that is exactly what appears to be happening here. What is going on?
Any consideration of a revolutionary proposal such as permanent arterial circulatory improvement resulting from intermittent pneumatic limb compression with persistence of benefits long after cessation of compression requires consideration of two issues: is it real, and how does it work. First, is it real. Prior anecdotal publications have suggested prolonged clinical benefits, but in the absence of persuasive data they were easily dismissed as wishful thinking on the part of gullible authors. Now we have a proper scientific study that cannot be so easily dismissed. The presented evidence is indeed persuasive. In fact, the walking benefit experienced by these patients with claudication far exceeds that described for the two drugs currently approved by the Food and Drug Admisistration for use in intermittent claudication: pentoxifylline and cilostazol. Of course, these patients were carefully selected. They all had claudication only, patent iliac arteries with superficial femoral artery occlusion, and perhaps most important, a patent popliteal artery. Interestingly, almost none of the patients had diabetes, a population far different from our usual patients with claudication. Nonetheless, the improvement in walking distance was indeed impressive. The improvement in ankle/brachial index and popliteal artery blood flow appears significant, although less impressive than the dramatic improvement in walking distance. A small concern here is that the control group experienced no improvement. In almost every drug study of claudication, a noticeable improvement in the control/placebo group has been noted (with the exception of cilostazol) presumably because of the learning that occurs with repeated treadmill walking. I have always had a built-in bias against studies that show no control/placebo improvement.
If we accept for the moment that these investigatiors have indeed observed a very important effect, what could possibly be the cause of the observed benefit? From the outset I reject a simple mechanical explanation. The laws of physics, especially conservation of energy, suggest to me that the circulatory deficiency during compression would only be balanced by enhanced flow during relaxation incident to venous emptying and refilling. Clearly there must be some other explanation. These authors suggest release of beneficial substances by that arterial (and venous?) endothelium. Perhaps nitric oxide or some other friendly nostrum may be involved, or perhaps suspension of the veno-arteriolar reflex by venous pressure reduction may be the important mechanism. Presently we clearly do not know.
Anecdotes have been accumulating long enough. The trial described in the study by Delis and associates is a step in the right direction; however, he had a control group but not a placebo group, his patients were carefully selected, and the number of patients was small. The time has clearly come for a multicenter, randomized trial. I suggest a proper placebo group that has the foot pneumatic device applied for the same number of hours per day as the treatment group, but with no pneumatic inflation. Perhaps some sort of vibration could be added to the limbs of the placebo group to simulate active treatment.
I do not know how well the device is tolerated, but the patient compliance reported by Dr. Delis was a remarkable 86%. If this device proves to be both effective and well tolerated, this could indeed represent a remarkable advance in our treatment of claudication. Patients could have the pneumatic device applied in the evening or even during sleep and expect more than 100% improvement in walking distance, with the improvement maintence for months after cessation of treatment. Presently we have no idea of the actual duration of benefits, if any, and the issue of reapplication of active treatment after 4 to 6 months of nonuse has not been addressed.
Please do not misunderstand my position. I am assuredly no enthusiast for this treatment, a position I clearly expressed previously.1 The whole thing still intuitively strikes me as a futile quest for a free lunch. However, based on to the evidence presented in the article by Delis and associates, it is fair to say that my attitude has changed from "ridiculous" to "maybe." It will behoove all of us to keep a careful, but critical, eye on this device. Who knows...it might work.
Reference:
1. Porter JM. Commentary. Year book of vascular surgery. St Louis: Mosby; 1996. p. 43.
Please see the related article by Dr. Konstantinos T. Delis, et al. J Vasc Surg 2000;31:650-61.
ACI Medical, LLC
1857 Diamond St.
San Marcos, CA 92078
Tel: (760) 744-4400 Fax: (760) 744-4401
Toll Free: 888 4 LEG FLO (4534356)
E-mail: info@acimedical.com
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Number 16
PNEUMATIC LIMB COMPRESSION: A FREE LUNCH? INVITED COMMENTS
John M. Porter, MD. Division of Vascular Surgery, Oregon Health Sciences University, Portland, OR
J Vasc Surg 2000;31:821-2
As the old adage reminds us, beware of something too good to be true: it probably is. The notion of obtaining permanent circulatory benefits in an ischemic limb by temporary intermittent pneumatic compression has been hovering around the edges of vascular practice for decades. The concept reemerged in recent years and now has a patina of scientific respectability by the article by Delis and associates in this issue of the Journal of Vascular Surgery.
I have historically dismissed this concept as non-sense: A quest for a perpetual motion machine, in fact, a free lunch. Long experience has taught that one rarely gets something for nothing, and that is exactly what appears to be happening here. What is going on?
Any consideration of a revolutionary proposal such as permanent arterial circulatory improvement resulting from intermittent pneumatic limb compression with persistence of benefits long after cessation of compression requires consideration of two issues: is it real, and how does it work. First, is it real. Prior anecdotal publications have suggested prolonged clinical benefits, but in the absence of persuasive data they were easily dismissed as wishful thinking on the part of gullible authors. Now we have a proper scientific study that cannot be so easily dismissed. The presented evidence is indeed persuasive. In fact, the walking benefit experienced by these patients with claudication far exceeds that described for the two drugs currently approved by the Food and Drug Admisistration for use in intermittent claudication: pentoxifylline and cilostazol. Of course, these patients were carefully selected. They all had claudication only, patent iliac arteries with superficial femoral artery occlusion, and perhaps most important, a patent popliteal artery. Interestingly, almost none of the patients had diabetes, a population far different from our usual patients with claudication. Nonetheless, the improvement in walking distance was indeed impressive. The improvement in ankle/brachial index and popliteal artery blood flow appears significant, although less impressive than the dramatic improvement in walking distance. A small concern here is that the control group experienced no improvement. In almost every drug study of claudication, a noticeable improvement in the control/placebo group has been noted (with the exception of cilostazol) presumably because of the learning that occurs with repeated treadmill walking. I have always had a built-in bias against studies that show no control/placebo improvement.
If we accept for the moment that these investigatiors have indeed observed a very important effect, what could possibly be the cause of the observed benefit? From the outset I reject a simple mechanical explanation. The laws of physics, especially conservation of energy, suggest to me that the circulatory deficiency during compression would only be balanced by enhanced flow during relaxation incident to venous emptying and refilling. Clearly there must be some other explanation. These authors suggest release of beneficial substances by that arterial (and venous?) endothelium. Perhaps nitric oxide or some other friendly nostrum may be involved, or perhaps suspension of the veno-arteriolar reflex by venous pressure reduction may be the important mechanism. Presently we clearly do not know.
Anecdotes have been accumulating long enough. The trial described in the study by Delis and associates is a step in the right direction; however, he had a control group but not a placebo group, his patients were carefully selected, and the number of patients was small. The time has clearly come for a multicenter, randomized trial. I suggest a proper placebo group that has the foot pneumatic device applied for the same number of hours per day as the treatment group, but with no pneumatic inflation. Perhaps some sort of vibration could be added to the limbs of the placebo group to simulate active treatment.
I do not know how well the device is tolerated, but the patient compliance reported by Dr. Delis was a remarkable 86%. If this device proves to be both effective and well tolerated, this could indeed represent a remarkable advance in our treatment of claudication. Patients could have the pneumatic device applied in the evening or even during sleep and expect more than 100% improvement in walking distance, with the improvement maintence for months after cessation of treatment. Presently we have no idea of the actual duration of benefits, if any, and the issue of reapplication of active treatment after 4 to 6 months of nonuse has not been addressed.
Please do not misunderstand my position. I am assuredly no enthusiast for this treatment, a position I clearly expressed previously.1 The whole thing still intuitively strikes me as a futile quest for a free lunch. However, based on to the evidence presented in the article by Delis and associates, it is fair to say that my attitude has changed from "ridiculous" to "maybe." It will behoove all of us to keep a careful, but critical, eye on this device. Who knows...it might work.
Reference:
1. Porter JM. Commentary. Year book of vascular surgery. St Louis: Mosby; 1996. p. 43.
Please see the related article by Dr. Konstantinos T. Delis, et al. J Vasc Surg 2000;31:650-61.
ACI Medical, LLC 1857 Diamond St. San Marcos, CA 92078 Tel: (760) 744-4400 Fax: (760) 744-4401 Toll Free: 888 4 LEG FLO (4534356) E-mail: info@acimedical.com |