Peripheral Vascular Disease

Peripheral vascular disease (PVD) refers to a variety of conditions that primarily affect the arteries of the body, with the exception of the coronary arteries that supply blood to the heart. (Those are covered in the article on cardiovascular disease.) The most common areas for PVD are the arteries of the legs and upper arms, the carotid (neck) arteries, the abdominal aorta and its branches, and the renal (kidney) arteries.

The cause of most types of PVD is hardening of the arteries (atherosclerosis), which itself has many causes. Conditions affecting the veins, such as chronic venous insufficiency, varicose veins, and hemorrhoids, are not usually included in PVD.

PVD of the carotid arteries is a major cause of stroke. Intermittent claudication refers to pain in the lower legs after walking short distances and is caused by PVD of the leg arteries. One cause of erectile dysfunction may be PVD of the penis. Raynaud’s disease is a painful condition caused by spasms of arteries after exposure to cold. Thromboangiitis obliterans (TAO), also known as Buerger’s disease, is an uncommon PVD that occurs in both arteries and veins. This condition causes tender areas of inflammation in the arms or legs, followed by cold hands or feet.

Aneurysm is a ballooning of an artery due to weakening of the blood vessel walls. Aneurysms may be an inherited disorder or may be due to atherosclerosis.¹ ² The most common aneurysm is abdominal aortic aneurysm (AAA), which occurs in the large artery that carries blood from the heart to the lower body. AAA is much more common in men, and risk increases with age. Large AAAs are usually surgically repaired because they can undergo life-threatening ruptures.

Medical treatments

Over the counter aspirin (Bayer Low Adult Strength®, Ecotrin Adult Low Strength®) may be recommended to prevent platelet aggregation and clotting.

Prescription drug treatment may include anti-platelet medications, such as clopidogrel (Plavix®), ticlopidine (Ticlid®), dipyridamole (Persantine®) and dipyridamol with aspirin (Aggrenox®), and cholesterol lowering drugs in combination with anti-claudication medications, such as cilostazol (Pletal®) and pentoxifylline (Trental®).

Exercise rehabilitation therapy, weight loss, and smoking cessation is often recommended. Healthcare providers might advise individuals to elevate their legs frequently, avoid prolonged standing or sitting, and wear graduated compression stockings with supportive shoes. Surgical options to restore blood supply (revascularization procedures, such as, angioplasty, atherectomy, stent placement, and bypass) are usually reserved for those with progressive or disabling symptoms. Any ulcers that develop are treated with compressive bandages that contain antibiotic solutions. Recurrent ulceration may be surgically treated with skin grafts and repair or bypass of the affected veins.

Nutritional supplements that may be helpful

As with other vascular diseases, people with TAO are more likely to have high levels of homocysteine and low levels of folic acid.⁴ However, no research has tested folic acid as prevention or treatment for this disease.

One controlled study compared a type of niacin (vitamin B3) known as inositol hexaniacinate to the drug pyridinolcarbamate for the treatment of skin ulcers caused by PVD.⁵ A placebo was not included in this trial, and both 1.2 grams daily of inositol hexaniacinate and 1.5 grams daily of the drug produced beneficial results in about half of the patients.

As in many vascular diseases, people with AAA often have abnormal cholesterol and triglyceride levels,⁶ and their blood vessel walls contain evidence of free radical damage.⁷ ⁸ However, it is not known whether lowering blood fats or taking free radical-destroying antioxidants will reduce the risk of AAA. The arterial walls of AAA are depleted of large molecules related to cartilage, including chondroitin sulfate,⁹ ¹⁰ but no research has investigated whether supplements of chondroitin sulfate might help prevent problems with AAA. Copper is required for normal artery structure.¹¹ Animal studies have shown that copper deficiency leads to weak aortic walls¹² and rupture of the aorta.¹³ Combating deficiency with copper supplements prevented rupture in an animal study.¹⁴ Copper deficiency in humans with AAA has been suggested in some studies,¹⁵ ¹⁶ but not in others.¹⁷ ¹⁸ ¹⁹ No studies have been done using copper supplements to prevent or manage aneurysms.

Are there any side effects or interactions?
Refer to the individual supplement for information about any side effects or interactions.

References

1. Anderson LA. An update on the cause of abdominal aortic aneurysms. J Vasc Nurs 1994;12:95–100 [review].

2. MacSweeney ST, Powell JT, Greenhalgh RM. Pathogenesis of abdominal aortic aneurysm. Br J Surg 1994;81:935–41 [review].

3. Szuba A, Cooke JP. Thromboangiitis obliterans. An update on Buerger’s disease. West J Med 1998;168:255–60 [review].

4. Stammler F, Diehm C, Hsu E, et al. The prevalence of hyperhomocysteinemia in thromboangiitis obliterans. Does homocysteine play a role pathogenetically? Dtsch Med Wochenschr 1996;121:1417–23 [in German].

5. Mishima Y, Kamiya K, Sakaguchi S, et al. A multiclinic double-blind trial of pyridinolcarbamate and inositol niacinate in ischemic ulcer due to chronic arterial occlusion. Angiology 1977;28:84–94.

6. Watt HC, Law MR, Wald NJ, et al. Serum triglyceride: a possible risk factor for ruptured abdominal aortic aneurysm. Int J Epidemiol 1998;27:949–52.

7. Killion SL, Hunter GC, Eskelson CD, et al. Vitamin E levels in human atherosclerotic plaque: the influence of risk factors. Atherosclerosis 1996;126:289–97.

8. Dubick MA, Hunter GC, Casey SM, Keen CL. Aortic ascorbic acid, trace elements, and superoxide dismutase activity in human aneurysmal and occlusive disease. Proc Soc Exp Biol Med 1987;184:138–43.

9. Theocharis AD, Tsolakis I, Tsegenidis T, Karamanos NK. Human abdominal aortic aneurysm is closely associated with compositional and specific structural modifications at the glycosaminoglycan level. Atherosclerosis 1999;145:359–68.

10. Sobolewski K, Wolanska M, Bankowski E, et al. Collagen, elastin and glycosaminoglycans in aortic aneurysms. Acta Biochim Pol 1995;42:301–7.

11. Hill CH. A role of copper in elastin formation. Nutr Rev 1969;27:99–100 [review].

12. Greene FL, Lamb LS, Barwick M, Pappas NJ. Effect of dietary copper on colonic tumor production and aortic integrity in the rat. J Surg Res 1987;42:503–12.

13. Vanhooser SL, Stair E, Edwards WC, et al. Aortic rupture in ostrich associated with copper deficiency. Vet Hum Toxicol 1994;36:226–7.

14. Guenthner E, Carlson CW, Emerick RJ. Copper salts for growth stimulation and alleviation of aortic rupture losses in turkeys. Poult Sci 1978;57:1313–24.

15. Tilson MD. Decreased hepatic copper levels. A possible chemical marker for the pathogenesis of aortic aneurysms in man. Arch Surg 1982;117:1212–3.

16. Tilson MD, Davis G. Deficiencies of copper and a compound with ion-exchange characteristics of pyridinoline in skin from patients with abdominal aortic aneurysms. Surgery 1983;94:134–41.

17. Senapati A, Carlsson LK, Fletcher CD, et al. Is tissue copper deficiency associated with aortic aneurysms? Br J Surg 1985;72:352–3.

18. Dubick MA, Hunter GC, Casey SM, Keen CL. Aortic ascorbic acid, trace elements, and superoxide dismutase activity in human aneurysmal and occlusive disease. Proc Soc Exp Biol Med 1987;184:138–43.

19. Jaakkola P, Hippelainen M, Kantola M. Copper and zinc concentrations of abdominal aorta and liver in patients with infrarenal abdominal aortic aneurysm or aortoiliacal occlusive disease. Ann Chir Gynaecol 1994;83:304–8.

20. Olszewer E, Carter JP. EDTA chelation therapy in chronic degenerative disease. Med Hypotheses 1988;27:41–9.

21. Chappell LT, Janson M. EDTA chelation therapy in the treatment of vascular disease. J Cardiovasc Nurs 1996;10:78–86.

22. Olszewer E, Sabbag FC, Carter JP. A pilot double-blind study of sodium-magnesium EDTA in peripheral vascular disease. J Natl Med Assoc 1990;82:173–7.

23. Guldager B, Jelnes R, Jorgensen SJ, et al. EDTA treatment of intermittent claudication—a double-blind, placebo-controlled study. J Intern Med 1992;231:261–7.

24. Van Rij AM, Solomon C, Packer SGK, Hopkins WG. Chelation therapy for intermittent claudication. A double-blind, randomized, controlled trial. Circulation 1994;90:1194–9.

25. Zheng P. Traditional Chinese medicine anesthesia in severe thromboangiitis obliterans. Report of 30 cases. Chin Med J (Engl) 1988;101(3):221–4.

26. Yang BH, Zhang SG. Study of thromboangiitis obliterans treated with “vascular no. 3” using Doppler ultrasound. Chung Hsi I Chieh Ho Tsa Chih 1989;9:596–8, 581 [in Chinese].

What are the symptoms of peripheral vascular disease?

Medical treatments

Lifestyle changes that may be helpful

Nutritional supplements that may be helpful

Holistic approaches that may be helpful

References