Cardiovascular responses during graded treadmill exercise in men with peripheral arterial disease and intermittent claudication.
Intermittent claudication is defined as fatigue, discomfort, or pain that occurs in specific lower limb muscle groups during effort as the result of exercise-induced ischemia that is usually relieved by rest (1). Although numerous diseases can cause intermittent claudication, the vast majority of patients with claudication have atherosclerotic peripheral arterial occlusive disease (PAD). PAD affects a large proportion of the general population, with an age-adjusted prevalence of approximately 12% and a prevalence of intermittent claudication of 3% to 7% (2). Claudication is associated with impairment of walking ability that adversely affects social, leisure, and occupational activities (3).
The prevalence of hypertension among patients with diagnosed PAD is 50-74% (4-7). Patients with either hypertension or PAD have a high risk of myocardial infarction and stroke, and when hypertension and PAD are both present, the risk is greatly increased (8-9). Compared with age-matched controls, individuals with PAD have a 7--to 10-fold higher risk of cardiovascular ischemic events, and short-term mortality is increased at least 3-fold (10). Hypertension increases the risk of intermittent claudication 2.5- to 4-fold in men and women, respectively, and the risk is proportional to the severity of hypertension (11). Svensson et al. (12) reported increased incidence of ST-depression in PAD patients during ambulatory monitoring in which heart rate and blood pressures averaged 103 bpm and 178/96 mmHg, respectively. Hypertension also contributes to the progression of atherosclerosis, the basic pathological process underlying PAD. Indeed, both hypertension and PAD are associated with abnormal levels of lipid and coagulation factors in the blood (13).
Resting and exercise hypertension in PAD participants has been documented in the literature (14-16). These authors have identified potential safety risks during exercise hypertension. However, the relationship of these variables to graded exercise intensities from rest to peak exercise has not been investigated.
Multiple factors influence cardiovascular responses to exercise in people with or without PAD. Muscular exercise, claudication and other discomforts, intrinsic pathology of PAD (ischemia and mitochondriopathy), the presence of multiple comorbidities such as diabetes and heart disease, advanced age, and physical deconditioning/inactivity (1) all likely contribute to the changes in cardiovascular responses to exercise.
The purpose of this study was to compare cardiovascular responses of participants with PAD and intermittent calf claudication to those of an aged-matched reference group of men without these conditions during graded treadmill exercise testing. We expected that cardiovascular responses (heart rate, HR; systolic blood pressure, SBP; diastolic blood pressure, DBP; and rate-pressure project, RPP) would be higher in magnitude and increase at a faster rate during graded exercise in participants with PAD and calf claudication than in a reference group of participants without PAD and claudication.
Participants: There were no clinically significant differences between PAD and non-PAD groups on mean age, height, body mass, and body mass index (Table 1). All PAD participants had an ABI [less than or equal to] 0.90 in at least one leg. However, groups differed substantially on ethnic composition, with the PAD group being predominately (52%) black and 40% white, and the non-PAD group being predominately (74%) white and 22% black.
All participants were recruited by convenience sampling and formed two groups: participants with PAD and intermittent calf claudication (PAD group, n = 48) and participants without PAD or claudication (non-PAD group, n = 23). All participants were male. The mean age, height, body mass, and body mass index of participants were 68 years, 178 cm, 85 kg, and 27 kg x [m.sup.-2], respectively. Descriptive characteristics of participants are detailed in Tables 1-4.
PAD participants were recruited from the Peripheral Vascular Clinic at a large urban tertiary care medical center for military veterans (VA West Los Angeles Healthcare Center, Los Angeles, CA). Participants without PAD were recruited from a local community fitness facility (n = 10), the PM&R General Clinic at the medical center (n = 10), and hospital staff (n = 3). Therefore, the non-PAD sample was composed of a mixture of sedentary and active elderly men. Prior to physical examination and review of medical history, the prospective participants signed an informed consent form that was approved by the medical center's Institutional Review Board. Participants were interviewed, examined, and cleared medically by a physician prior to participation.
The PAD group consisted of 48 veterans with moderate mobility impairment secondary to classic intermittent claudication in one or both gastrocnemius-soleus (calf) muscle groups (Fontaine stage IIa). PAD diagnosis was confirmed by the examining physician who used the Edinburgh Claudication Questionnaire (17) and ankle-brachial index (ABI) data in the prospective participant's medical record. Selection of the calf site for claudication was justified because PAD patients report it to be the most symptomatic muscle group during walking-induced intermittent claudication (18). All participants could walk at least 200 m nonstop safely without an assistive device. The exclusion criteria for the PAD group were as follows: claudication secondary to Buerger's disease, autoimmune arteritis, fibromuscular dysplasia, chronic and repetitive trauma, myofascial pain syndrome, venous stasis, hypercoagulability disorder, or arterial embolic disease; inability to perform treadmill walking safely at 2 mph; leg pain at rest, skin ulceration, necrosis or gangrene (Fontaine stage > IIa); poorly controlled diabetes mellitus (fasting blood sugar > 200 mg/dl or HbA1c > 9%); poorly controlled hypertension (resting BP > 160/100 mmHg); Raynaud's syndrome; changes in prescribed cardiovascular or pain medications within the past 6 months; exertional angina, dyspnea, fatigue, or dizziness; severe cardiopulmonary or other disease (NYHA classifications III or IV); myocardial infarction within the preceding 3 months; exercise intolerance limited by leg pain of nonvascular origin (e.g., arthropathy, neuropathy); transmetatarsal or more proximal lower-extremity amputation; nonambulatory in the last 6 months; severe leg weakness preventing leg exercise; surgery related to PAD during the preceding 3 months; unstable claudication symptoms during the preceding 3 months; terminal disease with < 6 months life expectancy; dementia (Folstein mini-mental state score < 24) (19). PAD participants had not been participating in regular exercise prior to testing, and were about to enter a clinical trial of exercise training to improve walking ability (20).
The non-PAD group consisted of 23 men with neither PAD nor any of the above exclusion criteria. Eleven non-PAD participants were veterans and twelve were nonveterans.
After medical examination, participants completed two questionnaires. The International Physical Activity Questionnaire (21) is a self-report of estimated the frequency and duration of vigorous, moderate, and walking activities in the past week and allows computation of the amount of weekly physical activity in MET x min x [week.sup.-1] (MET, metabolic equivalents, multiples of resting metabolic rate). The Walking Impairment Questionnaire (22) is a self-report of the effects of claudication on walking distance, speed, and stair-climbing ability, expressed as percentages of the maximal possible score if no impairment existed.
Procedures: All participants performed at least one treadmill test, with 27 PAD participants performing duplicate tests within a two-week period to assess reliability of measurements. For at least 3 hours before testing, participants were requested to take their physician-prescribed medications, and to refrain from over-the-counter pain medications, products with caffeine or nicotine, eating a heavy meal, or participating in strenuous physical activity.
Before exercise testing, participants completed two questionnaires to evaluate walking impairment and physical activity (previously described). Participants' height and body mass were measured on site; body mass index (kg x [m.sup.-2]) was calculated from height and body mass. ABI data of all veteran participants were retrieved from the most recent measurements in our medical center's computerized records; ABI data were unavailable for non-veterans.
All participants performed the standardized progressive Gardner-Skinner treadmill protocol (23) on a GE Marquette 2000 treadmill or GE T2100 treadmill. During the initial 5-minute pretest period, baseline brachial blood pressure, heart rate, and ECG rhythm and waveforms were obtained with the participant supine on a padded treatment table. Participants then immediately arose from the table and stood on the treadmill that began to move within seconds. The protocol involved a constant walking speed of 2 mph and an increase in grade of 2% every 2 minutes beginning at 0% grade (23) to a maximal possible grade of 14%. This protocol was symptom-limited for PAD participants, with the end point occurring when calf claudication became intolerable, as judged by the participant. Non-PAD participants performed the same protocol and all achieved the highest possible treadmill grade (14%). PAD participants rated the intensity of their calf claudication pain at the end of each minute of the test and at the end of exercise. We used the following validated 0-4 claudication pain rating scale: 0 = no pain, 1 = onset of pain, 2 = moderate pain, 3 = intense pain, and 4 = maximal/intolerable pain (24-25). If a participant reported intolerable pain or any other symptom of exercise intolerance, exercise was stopped immediately and he recovered in the supine position for at least 15 minutes until symptoms subsided and disappeared and cardiovascular responses returned to within 10% of pre-exercise levels.
Heart rate and ECG were monitored continuously with a GE Marquette Mac 8 or GE Case V6.51 12-lead ECG system, along with other symptoms of exercise intolerance. Brachial systolic and diastolic blood pressures were determined on the right arm by manual auscultation every two minutes during rest (minutes 1, 3, and 5), exercise, immediately after the last stage of exercise, and during recovery. All tests were directly medically supervised; standard precautions used in cardiac exercise testing were observed (26).
Outcome Measures: In PAD participants, cardiovascular variables and pain were determined at each test stage (treadmill grade) from rest until calf claudication became intolerable (i.e., pain = 4) and the protocol stopped. In non-PAD participants, all variables were determined during rest and all test stages from 0 to 14% grade; therefore the "peak" exercise responses were considered submaximal for non-PAD participants.
[FIGURE 1 OMITTED]
Cardiovascular measures were defined as follows:
* Heart rate (HR, bpm): Resting HR was the average HR during the last two minutes of the five-minute supine pre-exercise rest period. Peak HR was the highest average HR during a ten-second period during exercise, as determined from the 12-lead ECG report.
* SBP and DBP (mmHg): Resting SBP and DBP were the average of the second two SBP and DBP measurements, respectively, during the five-minute pre-exercise rest period. Peak SBP and DBP were the highest recorded SBP and DBP, respectively, during the test.
* RPP (bpm x mmHg x [10.sup.-3]): RPP was calculated as the product of HR and SBP, as defined above. RPP is directly proportional to the myocardial oxygen demand and cardiac work rate (27).
* Pain refers to the intensity of calf claudication discomfort reported by PAD participants who were monitored during and after exercise for its progression and dissipation, rated on the 0-4 scale previously mentioned.
Statistical Analyses: Descriptive statistics (mean, SD) were computed for all variables (except pain) for both groups at rest and peak exercise. Independent t-tests were used to compare mean descriptive and physiologic variables of the two groups at rest and (separately) during peak exercise. Linear regression was used to generate the regression slopes and other statistics for each cardiovascular variable during exercise. Additional independent t-tests were used to compare the groups on regression slopes. One-way repeated measures ANOVAs were performed between trials one and two for cardiovascular variables to generate the variance components necessary to compute the intraclass correlation coefficient ([ICC.sub.2,k]) to assess test-retest reliability of the outcome variables. In light of the 13 statistical hypotheses planned and tested, the Bonferroni correction was applied to maintain the experimentwise [alpha] level at 0.05 ([alpha] = 0.05 x [13.sup.-1] = 0.004). Additionally, four multiple regressions examined the possible influence of ethnic difference between groups on the slopes of the four cardiovascular variables vs. treadmill grade. NCSS 2005 (Kaysville, UT) statistical software was used to analyze all data.
The groups differed substantially on comorbidities and medication usage. The prevalence of nearly all comorbidities and PAD risk factors were much higher in the PAD group than in the non-PAD group (Table 2). The 48 PAD participants utilized 136 different prescriptions for medications to control HR and BP (average 2.8 per participant); two PAD participants took no medications. By contrast, the 23 non-PAD participants relied on 22 such prescriptions (average 1.0 per participant); nine non-PAD participants took no medications (Table 3).
The data for self-reported physical activity and walking impairment (Table 4) were non-normally distributed: negative skews for both groups for physical activity; positive skews and ceiling effects for non-PAD group for walking impairment variables). The PAD group's weekly physical activity, as estimated by the International Physical Activity Questionnaire, was significantly (62%) lower than that of the non-PAD group. The PAD group also reported significantly (47-67%) more walking impairment (i.e., distance, speed, and stair climbing) compared to the non-PAD group that had very little impairment.
Table 5 shows test-retest reliability data for each variable and group. Intraclass correlation coefficients ranged from 0.643 to 0.983, indicating moderate to high reliability. No clinically significant differences existed between trials one and two on any variable, so the average of both trials represented the criterion score for that variable. The variable with lowest reliability was DBP which does not vary widely across test stages.
Table 6 and Figure 1 illustrate differences between PAD and non-PAD groups for the four cardiovascular responses and pain during rest and peak exercise. During testing, non-PAD participants reported no specific pains, although exertion was considerable and fatigue was common in older and less fit participants. Groups had almost identical cardiovascular responses during supine pre-exercise rest periods. No participants reported calf pain during supine rest. During peak exercise, SBP, DBP, and RPP for the PAD group were significantly higher than the non-PAD group, although peak treadmill grade was 44% lower (6.5% vs. 14.0%, P < 0.001) with effect sizes for SBP and DBP rated as "large" and RPP rated as "medium".
All PAD participants completed at least two stages of treadmill walking (0% and 2% grades (estimated 2.5 and 3.1 METs). The mean [+ or -] SD time to peak exercise for PAD participants was 7.30 [+ or -] 4.10 minutes. All participants were limited by calf claudication symptoms (pain = 4/4). The PAD group achieved a mean [+ or -] SD peak treadmill grade of 6.5 [+ or -] 4.0% (range: 2-14%) and estimated peak MET level of 4.3 [+ or -] 1.1 METs (range: 2.5-6.4 METs).
By contrast, all non-PAD participants completed the treadmill testing protocol in the prescribed time limit of 16 minutes (estimated 6.4 METs). No non-PAD participants displayed signs or reported symptoms of pain or exercise intolerance severe enough to terminate the treadmill test. A one-sample t-test revealed that exercise time for the PAD group was significantly (54%) lower than that for the non-PAD group (P < 0.001).
Table 7 shows differences between groups in the slopes (rates of change) of cardiovascular variables with treadmill grade. All slopes were significantly higher for the PAD group (P > 0.001), with "large" effect sizes.
The most striking finding of this study was the markedly faster rate of increase of cardiovascular variables with increases in exercise intensity in the PAD compared to non-PAD groups. This was surprising in light of the nearly identical and normal responses during supine rest. While there is speculation about the physiological mechanisms behind these differences (not evaluated in this study), the severe and intolerable pain experienced by all PAD participants may be a major contributor at the higher exercise intensities. Additional research is required to elucidate the relative contributions of specific mechanisms. It has long been known that ischemia, pain, and exercise increase HR and BP by different additive mechanisms (28). One mechanism is feed forward "central command" and subsequent sympathetic outflow from the cardiovascular center in the midbrain to the heart and vasculature. This results in (a) increased heart rate and contractility, and (b) the pressor response (increased arterial BP) from peripheral vasoconstriction and increased vascular resistance in the less active muscular and visceral vasculature. Peripheral feedback mechanisms (carotid chemoreceptors, respiratory muscle receptors, and limb locomotor muscle group III-IV afferents) enhance the sympathetically mediated pressor response (29). It has also been known that normal resting BP may underestimate ambulatory/exercise BP (30) in healthy people. These findings are clearly supported by the data in the present study.
Ritti-Dias et al. (16) reported mean cardiovascular responses of 79 PAD participants during pre-exercise rest and at/near peak treadmill exercise. Despite our data being recorded with participants in supine posture, our BP data are nearly identical to their data while participants stood upright. However, the data in the present study our HR and RPP data were on average 15% lower than in the Ritti-Dias et al. study due to the increased cardiac preload associated with supine posture. Ritti-Dias et al. (16) also reported mean peak HR, SBP, DBP, and RPP in PAD participants reached 121 bpm, 155/85 mmHg, and 18.8 bpm x mmHg x [10.sup.-3], respectively, at completion of the Gardner-Skinner treadmill test protocol (also used in this study) that elicited maximal tolerable pain after an average of 11 minutes of walking during which the peak treadmill grade reached 10%. Although their peak DBP values were similar to those reported in the current study, our HR, SBP, and RPP values were higher (by 6[degrees]%, 14%, and 8%, respectively), despite the higher prevalence of [beta]-blocker medication usage in our sample (60% vs. 34%). The cardiovascular differences may have been related to the 33% lower ABI values in our sample (0.61 vs. 0.81), indicating more severe PAD and suggesting systemic atherosclerosis (31-35).
RPP in particular has relevance to PAD patients with concomitant ischemic heart disease, as it is directly proportional to the myocardial oxygen consumption and cardiac work rate (26). RPP at the onset of angina pectoris is reproducible in a given patient with coronary artery disease (36); hence, RPP needs to be monitored during exercise in PAD patients.
Tables 1-2 show that the PAD and non-PAD groups were nearly identical in physical size, but very different in comorbidities, PAD risk factors, cardiovascular medication usage, physical activity, and walking impairment. The differences reflect the typical veteran PAD population described in the literature (37); claudication symptoms may have a greater impact on functional walking than other comorbidities of milder severity. Although not measured in this study, it is well established that the average V[O.sub.2]peak of the PAD population is about 50% that of non-PAD population (38-40). Therefore, some of the differences in cardiovascular responses during exercise between groups were probably attributable to differences in levels of aerobic and cardiovascular fitness (35) which result from lower physical activity and the burden of multiple comorbidities.
Because ethnicity was not balanced between groups, the possibility exists that the higher prevalence of blacks in the PAD group could explain their higher cardiovascular responses. However, the four multiple regression analyses indicated that ethnicity was unrelated (P > 0.05) to the slopes of the four cardiovascular variables vs. treadmill grade. Collins et al. (41) found a higher prevalence of PAD among black men compared to white or Latino men in a large sample including many American veterans (N=403). However, after adjusting for education and atherosclerotic risk factors (age, smoking, diabetes, hypertension), ethnicity was nof an independent risk factor for PAD.
Table 6 compares mean cardiovascular responses of the two groups at rest and during peak exercise. The resting responses of the groups were within normal limits and very similar, despite the differences in comorbidities, physical activity, and presumably fitness level. No other published data could be found with which to compare these responses to non-PAD reference groups. Figure 1 illustrates the linear relationships between each cardiovascular variable and treadmill grade for each group, with linear regression equations and related statistics.
A normal increase in HR during aerobic exercise is 10 bpm/MET (26). The average peak MET level for PAD participants was 4.3 METs, or 3.3 METs above the resting level. This would suggest the cutoff for normal HR increase during exercise would be 101 bpm, somewhat lower than the 111-bpm average for peak HR of PAD participants, even though they took more [beta]-blocking medications and experienced substantial claudication pain through recovery minute 4.
A normal increase in SBP during aerobic exercise is 10 mmHg/MET (26). The average peak MET level for PAD participants was 4.3 METs, or 3.3 METs above the resting level. This would suggest the cut-off for normal SBP increase during exercise would be 166 mmHg, very similar to the 170-mmHg average for peak SBP of PAD participants, even though they took more [beta]-blocking medications and experienced substantial claudication pain through recovery minute 4.
Normal responses of DBP to aerobic exercise are either no change or a small decrease (26). The DBP of 41/50 (82%) of PAD participants increased during exercise, while that of non-PAD increased in only 7/23 (30%). No participants reached or exceeded the DBP end-point during testing, i.e., abnormal DBP of 115 mmHg. Among PAD participants, eight recorded increases in DBP >15.0 mmHg and nine others had increases of 13.0-14.5 mmHg; only one non-PAD participant exceeded the 15-mmHg increase limit.
Because the cardiovascular system responds to and supports increases in metabolic demand, cardiovascular responses are traditionally expressed as a function of oxygen consumption (V[O.sub.2]) or METs. These responses during exercise are usually assumed to represent physiologic steady-state conditions (39). However, the 2-minute stages of the treadmill test protocol were too short to allow for a physiologic steady-state at each grade (42). Therefore, the results represent non-steady conditions, but should be similar to what clinicians would observe when they had monitored PAD patients during the standardized Gardner-Skinner treadmill test protocol.
Peak treadmill exercise induced substantially higher BPs and RPP in the PAD group than in the non-PAD group. This was surprising in light of the shorter exercise time, lower peak treadmill grade, and beta-blocker usage among 60% of the PAD participants.
Compared to 4% of non-PAD participants, 96% of PAD participants took [[beta].sub.1] antagonists, angiotensin-converting enzyme inhibitors, diuretics, and/or calcium-channel blockers which act to decrease HR and/or BP. A remarkable finding of this study is the exaggerated chronotropic and hypertensive responses of PAD participants during exercise despite the many medications prescribed to control HR and BP. Although controlled at rest, these medications failed to control HR and BP during painful exercise. Use of [[beta].sub.2] agonists (for treatment of chronic obstructive pulmonary disease) in seven PAD participants may have contributed to their higher HR and BP responses.
All PAD participants had diagnosed PAD, i.e., ABI [less than or equal to] 0.90 in at least one leg. However, ABI was not assessed in the non-PAD group; therefore, we cannot be certain that some non-PAD participants did not have subclinical PAD, especially since several of the 24 non-PAD participants had CAD and PAD risk factors (Table 2). If PAD was underestimated in the non-PAD group, then the differences in cardiovascular responses between groups may have been even greater than reported, supporting our general findings to a greater degree.
In light of the role of exercise in the treatment of PAD patients, future research may involve determination of specific causes of and methods to control hypertensive responses to exercise and claudication pain in PAD participants.
In conclusion, treadmill exercise induced higher levels of cardiovascular stress in the PAD group with claudication than in the non-PAD group. Cardiovascular variables (HR, SBP, DBP, RPP) increased at a faster rate with increasing treadmill grade and metabolic demand.
Clinical Implications: Clinicians are advised to observe strict cardiac precautions when exercising this population because of the higher incidence of concomitant CAD and higher cardiovascular responses associated with painful walking/exercise in PAD patients.
This project was supported in part by grant # B3644P from the Rehabilitation Research and Development Service, Department of Veterans Affairs to Drs. Figoni and A. M. E. Scremin.
We thank the Physical Medicine and Rehabilitation Service at the VA West Los Angeles Healthcare Center for the use of staff, facilities, equipment, and supplies.
CONFLICT OF INTEREST
The authors have no professional relationships with companies, manufacturers who will benefit from the results of the present study. The results of the present study do not constitute endorsement of a product by the AKTA. No conflicts of interest have been reported by the authors or by any individuals in control of the content of this article. None of the authors benefitted financially from the research or have any conflict of interest.
This study was presented at the 2011 Annual Meeting of the American College of Sports Medicine, Denver, CO. A similar abstract is published as follows:
Figoni, S. F., C. F. Kunkel, A. C. Phillips, and A. M. E. Scremin. Cardiovascular responses during treadmill exercise in men with peripheral arterial disease and intermittent claudication. Med Sci Sporfs Exerc 43(5, Suppl.):S527, 2011.
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Stephen F. Figoni, PhD, RKT
VA West Los Angeles Healthcare Center
11301 Wilshire Blvd.
Los Angeles, CA 90073
Phone: (310) 478-3711, x40676
FAX: (310) 268-4935
Stephen F. Figoni, PhD, RKT [a], Charles F. Kunkel, MD, MS [a,b], Amanda C. Phillips, MS [a], A. M. Erika Scremin, MD [a,b]
[a] Physical Medicine and Rehabilitation Service, VA Greater Los Angeles Healthcare System (VAGLAHS), West Los Angeles Healthcare Center (WLAHC), Los Angeles, CA; [b] Physical Medicine and Rehabilitation Division, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA
Table 1. Mean [+ or -] SD demographic and descriptive data in peripheral arterial disease (PAD) and non-PAD groups. Non-PAD (n = 23) PAD (n = 48) Age (yr) 68.1 [+ or -] 9.2 68.7 [+ or -] 9.2 Height (cm) 177.9 [+ or -] 7.7 177.9 [+ or -] 7.0 Body mass (kg) 86.7 [+ or -] 11.5 85.7 [+ or -] 16.6 Body mass index 27.4 [+ or -] 2.7 27.0 [+ or -] 4.4 (kg x [m.sup.-2) Ankle-brachial -- 0.61 [+ or -] 0.14 index Ethnicity n % n % Black 5 22 25 52 White 17 74 19 40 Hispanic, non- 0 0 3 6 Caucasian Native American 0 0 1 2 Asian/Pacific 1 4 0 0 Islander Table 2. Prevalence of comorbidities, PAD risk factors, and medications in peripheral arterial disease (PAD) and non-PAD groups. Non-PAD (n = 23) PAD (n = 48) n % n % Hypertension 9 39 45 94 Hyperlipidemia 12 52 37 77 Past smoking 6 26 37 77 Coronary artery disease 5 22 29 64 Diabetes mellitus 0 0 24 50 Obesity 4 17 17 35 Current smoking 0 0 14 29 Chronic renal insufficiency 1 4 12 25 Stroke 1 4 11 23 Congestive heart failure 1 4 11 23 Leg vascular bypass surgery 0 0 10 21 Peripheral neuropathy 0 0 7 15 Chronic obstructive pulmonary disease 1 4 7 15 Table 3. Prevalence of cardiovascular medications in peripheral arterial disease (PAD) and non-PAD groups. Effect Effect on HR on BP [[beta].sub.1] [down arrow] [down arrow] antagonist ACE inhibitor -- [down arrow] Diuretic -- [down arrow] Calcium-channel [down arrow] [down arrow] blocker [[beta].sub.2] [up arrow] [up arrow] agonist (inhalers) No cardiovascular medications Non-PAD (n = 23) PAD (n = 48) n % n % [[beta].sub.1] 2 4 36 75 antagonist ACE inhibitor 10 21 34 71 Diuretic 4 8 24 50 Calcium-channel 5 10 21 44 blocker [[beta].sub.2] 0 0 7 15 agonist (inhalers) No cardiovascular 9 39 2 4 medications HR = heart rate, BP = arterial blood pressure, ACE = angiotensin-converting enzyme Table 4. Questionnaire-based descriptive data (median [+ or -] semi-interquartile range, minimum-maximum) on physical activity (from International Physical Activity Questionnaire) and walking impairment (from Walking Impairment Questionnaire) for peripheral arterial disease (PAD) and non-PAD groups. Non-PAD PAD (n = 48) [DELTA] (n = 23) Physical activity 2193 [+ or -] 814 [+ or -] -1378 (MET x min 1994, 330-9702 689, 0-6984 x [wk.sup.-1]) Walking impairment 100 [+ or -] 53 [+ or -] -47 (distance) 0, 93-100 29, 0-95 Walking impairment 100 [+ or -] 33 [+ or -] -67 (speed) 7, 29-100 15, 0-91 Walking impairment 100 [+ or -] 37 [+ or -] -63 (stairs) 4, 50-100 30, 0-100 % [DELTA] P ([dagger]) Physical activity -62 <0.001 (MET x min x [wk.sup.-1]) Walking impairment -47 <0.000 (distance) Walking impairment -67 <0.000 (speed) Walking impairment -63 <0.000 (stairs) MET, metabolic equivalent or multiple of resting metabolic rate. * Walking impairment scores are expressed as a percentage of maximal possible values; a lower score indicates more impairment. %[DELTA] represents difference from non-PAD group. ([dagger]) P-values for Mann-Whitney U-tests Table 5. Intraclass correlation coefficients (model 2,k) reflecting test-retest reliability of cardiovascular variables during supine rest and peak treadmill exercise for 27 peripheral arterial disease (PAD) participants and 23 non-PAD participants who submitted to duplicate testing. Non-PAD PAD (n = 23) (n = 27) Supine rest Heart rate 0.712 0.875 Systolic blood 0.692 0.812 pressure Diastolic blood 0.787 0.911 pressure Rate-pressure 0.829 0.775 product Peak exercise Heart rate 0.880 0.763 Systolic blood 0.983 0.686 pressure Diastolic blood 0.643 0.831 pressure Rate-pressure 0.807 0.727 product Table 6. Mean [+ or -] SD cardiovascular responses for peripheral arterial disease (PAD) and non-PAD groups during treadmill exercise tests. Non-PAD PAD [DELTA] (n = 23) (n = 48) Supine rest Heart rate (bpm) 68 [+ or -] 67 [+ or -] -0 10 11 Systolic blood 125 [+ or -] 132 [+ or -] 7 pressure (mmHg) 11 18 Diastolic blood 75 [+ or -] 74 [+ or -] -1 pressure (mmHg) 7 10 Rate-pressure product 8.5 [+ or -] 8.8 [+ or -] -0.4 (bpm x mmHg x 1.3 1.8 [10.sup.-3]) Peak exercise Exercise time 16 [+ or -] 7.30 [+ or -] -8.70 (min) 0 4.10 Treadmill grade (%) 14 [+ or -] 6.5 [+ or -] -7.5 0 4.0 Heart rate (bpm) 116 [+ or -] 114 [+ or -] -2 11 17 Systolic blood 156 [+ or -] 177 [+ or -] 21 pressure (mmHg) 15 24 Diastolic blood 69 [+ or -] 84 [+ or -] 15 pressure (mmHg) 11 14 Rate-pressure product 18.1 [+ or -] 20.2 [+ or -] 2.1 (bpm x mmHg x 2.8 4.9 [10.sup.-3]) %[DELTA] P d ([double dagger]) Supine rest Heart rate (bpm) -1 * * Systolic blood 5 pressure (mmHg) Diastolic blood -2 pressure (mmHg) Rate-pressure product -4 (bpm x mmHg x [10.sup.-3]) Peak exercise Exercise time -54 <0.000T 1.57 (min) Treadmill grade (%) -44 <0.000T 1.85 Heart rate (bpm) -0.0 * 0.13 Systolic blood 18 <0.001 1.07 pressure (mmHg) Diastolic blood 14 <0.001 1.16 pressure (mmHg) Rate-pressure product 18 <0.001 0.53 (bpm x mmHg x [10.sup.-3]) P values refer to independent t-tests, except for Exercise time and Treadmill grade, where one-sample t-tests were used. * non-clinically significant differences between groups ([dagger]) All non-PAD participants completed the treadmill test protocol to 14% grade in the maximum time of 16 minutes. ([double dagger]) d = Cohen's d (effect size): 0.2-0.3 "small", 0.5 "medium", [greater than or equal to] 0.8 "large" Table 7. Mean [+ or -] SD linear regression slopes of treadmill grade on cardiovascular variables for peripheral arterial disease (PAD) and non-PAD groups. Non-PAD PAD (n = 48) (n = 23) Heart rate (bpm) 196 [+ or -] 46 359 [+ or -] 230 Systolic blood 1.79 [+ or -] 0.70 6.3 [+ or -] 4.6 pressure (mmHg) Diastolic blood -0.21 [+ or -] 0.56 1.25 [+ or -]1.55 pressure (mmHg) Rate-pressure product 469 [+ or -] 134 1262 [+ or -] 830 (bpm x mmHg x [10.sup.-3]) P * d ([dagger]) Heart rate (bpm) <0.001 0.79 Systolic blood <0.001 1.04 pressure (mmHg) Diastolic blood <0.001 1.00 pressure (mmHg) Rate-pressure product <0.001 1.02 (bpm x mmHg x [10.sup.-3]) * P values for independent f-tests (Aspin-Welch unequal-variance test) ([dagger]) d = Cohen's d (effect size): 0.2-0.3 "small", 0.5 "medium", [greater than or equal to] 0.8 "large"
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|Author:||Figoni, Stephen F.; Kunke, Charles F.; Phillips, Amanda C.; Scremin, Erika A.M.|
|Publication:||Clinical Kinesiology: Journal of the American Kinesiotherapy Association|
|Date:||Sep 22, 2012|
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