In 1999/2000, about 6.3 million people experienced symptoms of intermittent claudication. On average, about 1750 new cases are diagnosed each year in this population. This survey provides a benchmark with respect to rates from past studies and emphasizes the need for more comprehensive research and for national surveillance in order to develop and evaluate treatment strategies.
A person with a clinical diagnosis of claudication should receive appropriate workup with a vascular consultation. The following signs will most frequently trigger a vascular consultation:\n- Resting limb pain.\n- Pain with activity: walking or rising from a chair.\n- Symptoms such as erythema, ischemia, and/or swelling.\n- Muscle tenderness.\n- Dyspnea or fatigue and decreased lung volume.\n- Tachycardia.
This survey confirms the prevalence of ICl and the poor outcome of the disease, with a 6-year survival of less than 10%. Thus, in our patients, ICl is a deadly disease. There is no cure for IT.
The clinical presentation of intermittent claudication may be multifactorial, including peripheral vascular disease, the muscular or subcutaneous anatomy of the upper legs and lower back, aortofemoral compression and nerve root compression secondary to aortic enlargement.
Intermittent claudication (IC) is the most common form of peripheral arterial disease (PAD). IAT in combination with other therapies is the preferred treatment of choice. When IAT is performed in conjunction with vasoactive agents, percutaneous transluminal angioplasty is the only intervention that can offer prolonged and complete relief. This treatment modality is very effective, less costly and much less invasive than surgery, especially for the elderly. In addition to IAT, other interventions including pneumatic compression devices, leg pumping devices (ex.
In a population study of patients with intermittent claudication, there were significant differences in health status, prevalence of heart disease, and type of claudication between men and women. Because of the confounding effect that health status had on the relationship between claudication and sex in our analysis, we were unable to clarify the potential role of sex in the etiology of intermittent claudication.
The side effects of l-ascorbate were frequent, most of which were minor in nature. The most common side effect in our study was palpitations. It is worth considering in patients with cardiovascular disease and the frequent use of this drug in a clinical setting. Further investigation of the indications and side effects are required.
Patients with disabling unilateral or bilateral chronic intermittent claudication should participate in medical evaluations before starting a clinical trial. This should include a careful evaluation for the need for revascularization, peripheral artery vasomotor or sensory neuropathy, and/or autonomic neuropathy.
In a retrospective review, patients who underwent bypass for intermittent claudication were not seen any less frequently postvascular intervention than patients who underwent surgery for carotid narrowing - contrary to previously reported rates. With appropriate patient selection, symptomatic intermittent claudication can be treated effectively.
In the setting of intermittent claudication, ascorbic acid dosages between 2 and 3 g/day have no significant long-term effect on arterial stiffness or function or on the incidence of cardiovascular events. Large scale multicenter placebo studies are required to investigate the potential risks of ascorbic acid in this setting.
Intermittent claudication in both the father and brother were more common than in the controls. Given the high prevalence of IC in the family members, IC as an early symptom of PD should be given serious consideration. The close association between IC and the mother is especially interesting. These observations support a probable hereditary component in the genesis of IC.
Plasma concentrations of L-ascorbic acid were low compared to those reported in a previous study in claudicants using oral glucose tablets with normal fasting L-ascorbic acid levels of 3.7 +/- 0.6 mg/dL.