Lower Extremity Arterial Disease and Lumbar Spinal Stenosis: A Study of Exercise-Induced Arterial Ischemia in 5197 Patients Complaining of Claudication.

Only few studies have analyzed the associations of lower extremity artery disease (LEAD) with lumbar spinal stenosis (LSS), although it is expected to be a frequent association. With exercise-oximetry, we determined the presence of exercise-induced regional blood flow impairment (ischemia) in 5197 different patients complaining of claudication and referred for treadmill testing. We recorded height, weight, age, sex, ongoing treatments, cardiovascular risk factor (diabetes, high blood pressure, current smoking habit), and history of suspected or treated LSS and/or lower limb revascularization. An ankle-brachial index at rest < 0.90 or >1.40 on at least one side was considered indicative of the presence of LEAD (ABI+). Ischemia was defined as a minimal DROP (Limb-changes minus chest-changes from rest) value < −15 mmHg during exercise oximetry. We analyzed the clinical factors associated to the presence of exercise-induced ischemia in patients without a history of LSS, using step-by-step linear regression, and defined a score from these factors. This score was then tested in patients with a history of LSS. In 4690 patients without a history of (suspected, diagnosed, or treated) LSS, we observed that ABI+, male sex, antiplatelet treatment, BMI< 26.5 kg//m2, age ≤ 64 years old, and a history of lower limb arterial revascularization, were associated to the presence of ischemia. The value of the score derived from these factors was associated with the probability of exercise-induced ischemia in the 507 patients with a history of LSS. This score may help to suspect the presence of ischemia as a factor of walking impairment in patients with a history of lumbar spinal stenosis.

Relationship Between the Severity of Exercise Induced Ischaemia and the Prevalence of Exercise Induced Calf Symptoms During Treadmill Testing With Transcutaneous Oximetry.

OBJECTIVE: It was hypothesised that there is a linear relationship between the severity of exercise induced calf ischaemia and the prevalence of calf claudication on a treadmill until a plateau is reached. It was expected that no pain would be present in the absence of ischaemia and all severely ischaemic calves would be symptomatic. METHODS: This was a retrospective analysis of a cross sectional acquired database recording. Transcutaneous oxygen pressure (TcPO2) on the chest and on each calf was used to evaluate calf ischaemia during treadmill tests with simultaneous recording of calf pain in 7 884 subjects (15 768 calves). The minimum value of calf changes from rest minus chest changes from rest (DROPm) was calculated. Regression analyses were used to determine the correlation between the proportion of exercise induced symptoms present in the calves and each unit of DROPm values. Analysis was repeated after objective determination of the cutoff point between the linear increase and the plateau. RESULTS: A linear relationship was found between the degree of ischaemia and the proportion of symptomatic calves for DROPm values ranging from 0 mmHg to -28 mmHg (proportion = -0.014 × DROPm + 0.32, r = 0.961, p <.001). For DROPm values lower than -28 mmHg (severe ischaemia), on average one of three limbs remained asymptomatic. The biphasic relationship between DROPm and prevalence of symptoms persists after exclusion of patients with diabetes mellitus, exercise induced hypoxaemia, and no evidence of lower extremity arterial disease (LEAD). CONCLUSION: The relationship between exercise induced pain and ischaemia is biphasic with a linear increase in the proportion of symptomatic limbs with ischaemia severity, until a plateau is reached for the more severely ischaemic limbs. The presence of exercise related calf symptoms should not automatically be reported as indicating the presence of LEAD; and the absence of exercise induced symptoms is not proof that ischaemia does not occur during exercise.

Identification of new factors associated to walking impairment in patients with vascular-type claudication.

OBJECTIVES: Mechanisms of walking limitation in arterial claudication are incompletely elucidated. We aimed to identify new variables associated to walking limitation in patients with claudication. METHODS: We retrospectively analyzed data of 1120 patients referred for transcutaneous exercise oxygen pressure recordings (TcpO2). The outcome measurement was the absolute walking time on treadmill (3.2 km/h, 10% slope). We used both: linear regression analysis and a non-linear analysis, combining support vector machines and genetic explanatory in 800 patients with the following resting variables: age, gender, body mass index, the presence of diabetes, minimal ankle to brachial index at rest, usual walking speed over 10 m (usual-pace), number of comorbid conditions, active smoking, resting heart rate, pre-test glycaemia and hemoglobin, beta-blocker use, and exercise-derived variables: minimal value of pulse oximetry, resting chest-TcpO2, decrease in chest TcpO2 during exercise, presence of buttock ischemia defined as a decrease from rest of oxygen pressure index ≤15 mmHg. We tested the models over 320 other patients. RESULTS: Independent variables associated to walking time, by decreasing importance in the models, were: age, ankle to brachial index, usual-pace; resting TcpO2, body mass index, smoking, buttock ischemia, heart rate and beta-blockers for the linear regression analysis, and were ankle to brachial index, age, body mass index, usual-pace, decrease in chest TcpO2, smoking, buttock ischemia, glycaemia, heart rate for the non-linear analysis. Testing of models over 320 new patients gave r = 0.509 for linear and 0.575 for non-linear analysis (both p < 0.05). CONCLUSION: Buttock ischemia, heart rate and usual-pace are new variables associated to walking time.