Peripheral artery disease (PAD) is one of the most common cardiovascular diseases. Despite high prevalence of PAD, data regarding the dietary patterns of Canadian individuals with PAD is required. Biomarkers are used as an alternative to dietary assessment methods and are generally used to measure true dietary intake. A total of 30 participants with established PAD were recruited for this study. Dietary intakes were estimated using a 3 day food record (3DFR) and food frequency questionnaire (FFQ). Docosahexaenoic acid (DHA) status was analyzed in plasma, plasma PL and RBC membrane PL. The determined mean dietary macronutrient distribution consisted of 18% protein, 33% fat and 47% carbohydrate with 3DFR and 19% protein, 36% fat and 43% carbohydrate with FFQ. The mean intakes using 3DFR and FFQ, respectively, were: saturated fat = 24.2, 22.8 g; sodium = 4156.6, 2852.3 mg; eicosapentaenoic acid (EPA) = 90.0, 50.0 mg and DHA = 128.5, 110.0 mg. FFQ showed significant (p<0.05) correlation (r=0.48) with plasma and plasma PL DHA. As compared to national guidelines, the participants consumed a diet that was 61% higher than National Cholesterol Education Program (NCEP) recommendations for saturated fat. Also, the participants consumed a diet which was 177% and 246% higher than NCEP and the Institute of Medicine (IOM) recommendations for sodium, respectively. Hence, PAD patients should be encouraged to eat a diet that is lower in saturated fat and sodium. None of the participants met the American Heart Association (AHA) recommendations for established cardiovascular disease of 1g of combined EPA and DHA.

Peripheral artery disease (PAD) is one of the most common cardiovascular diseases. Despite high prevalence of PAD, data regarding the dietary patterns of Canadian individuals with PAD is required. Biomarkers are used as an alternative to dietary assessment methods and are generally used to measure true dietary intake. A total of 30 participants with established PAD were recruited for this study. Dietary intakes were estimated using a 3 day food record (3DFR) and food frequency questionnaire (FFQ). Docosahexaenoic acid (DHA) status was analyzed in plasma, plasma PL and RBC membrane PL. The determined mean dietary macronutrient distribution consisted of 18% protein, 33% fat and 47% carbohydrate with 3DFR and 19% protein, 36% fat and 43% carbohydrate with FFQ. The mean intakes using 3DFR and FFQ, respectively, were: saturated fat = 24.2, 22.8 g; sodium = 4156.6, 2852.3 mg; eicosapentaenoic acid (EPA) = 90.0, 50.0 mg and DHA = 128.5, 110.0 mg. FFQ showed significant (p<0.05) correlation (r=0.48) with plasma and plasma PL DHA. As compared to national guidelines, the participants consumed a diet that was 61% higher than National Cholesterol Education Program (NCEP) recommendations for saturated fat. Also, the participants consumed a diet which was 177% and 246% higher than NCEP and the Institute of Medicine (IOM) recommendations for sodium, respectively. Hence, PAD patients should be encouraged to eat a diet that is lower in saturated fat and sodium. None of the participants met the American Heart Association (AHA) recommendations for established cardiovascular disease of 1g of combined EPA and DHA.

Although poor walking is the most common symptom of peripheral artery disease (PAD), reported results are inconsistent when comparing gait parameters between PAD patients and healthy controls. This inconsistency may be due to frailty, which is highly prevalent among PAD patients. To address this hypothesis, 41 participants, 17 PAD (74 +/- 8 years) and 24 aged-matched controls (76 +/- 7 years), were recruited. Gait was objectively assessed using validated wearable sensors. Analysis of covariate (ANCOVA) tests were used to compare gait parameters between PAD and non-PAD groups, considering age, gender, and body mass index as covariates, while stratified based on frailty status. According to the Fried frailty index, 47% of PAD and 50% of control participants were non-frail and the rest were classified as pre-frail. Within non-frail participants, gait speed, body sway during walking, stride length, gait cycle time, double-support, knee range of motion, speed variability, mid-swing speed, and gait initiation were significantly different between PAD and control groups (effect size d = 0.75 +/- 0.43). In the pre-frail group, however, most of the gait differences were diminished except for gait initiation and gait variability. Results suggest that gait initiation is the most sensitive parameter for detecting gait impairment in PAD participants when compared to controls, regardless of frailty status (d = 1.30-1.41; p<0.050). The observed interaction effect between frailty and PAD on gait parameters confirms the importance of assessing functionality in addition to age to provide more consistency in detecting motor performance impairments due to PAD.

No description available.

Peripheral artery disease (PAD) is associated with increased risk for arterial thromboembolic events, and antithrombotic therapy is fundamental to its treatment. Females with PAD have unique characteristics that impact their disease experience, but data is lacking on the differential effects of antithrombotic regimens in females with PAD. We developed a protocol and conducted two systematic reviews and meta-analyses to 1) assess the impact of female sex on cardiovascular, limb, and bleeding events in antithrombotic trials enrolling PAD patients, and 2) evaluate the representation of female PAD patients in antithrombotic trials, as well as trial generalizability. Females did not confer any benefit from dual antiplatelet therapy, dual pathway inhibition, or therapeutic oral anticoagulation over mono-antiplatelet therapy alone, however trial generalizability was limited by poor female enrolment and insufficient sex-based analyses. A more tailored approach to secondary prevention in females with PAD (beginning with improved study design) may yield better outcomes.

The absence of a practice guideline for peripheral artery disease (PAD) in the cardiology department creates differing practice preferences among providers, leading to deviations in practice among staff. Variations in practice can affect the quality of care that is provided to patients. This project was guided by research statements indicating that there was a difference in the screening approach for PAD among health practitioners at preimplementation and postimplementation and that an 85% compliance with the guideline would signify consistency in the provision of care. Rogers' theory of diffusion of innovations was used to facilitate the adoption of the guideline. This project helped close the gap between research (adoption of a guideline) and practice (compliance in the use of evidence in clinical practice). Using random medical record reviews and pretest-posttest design, the results of the project showed that patterns of using the PAD guideline in practice at preimplementation significantly differed compared to postimplementation. The rates of screening for the compliance of the PAD guideline showed approximately an eightfold increase. The adoption of the PAD guideline has implications for policy, because adopting the PAD guideline helped standardize the care, improve effectiveness of care in nursing practice, evaluate quality through use of research, and promote social change by improving patient outcomes.

Peripheral artery disease (PAD) affects 8 to 10 million Americans, and the incidence of PAD is expected to increase as the population ages. A high percentage of the PAD is undiagnosed prior to the onset of a serious cardiovascular event; therefore, the inability to screen and diagnose for PAD in the early stages could hinder efforts to decrease adverse consequences of cardiovascular disease. Individuals with PAD have a 3 to 5 times increased risk of cardiovascular disease (CVD) mortality when compared to people without PAD. Guided by the Stetler model, the purpose of this project was to evaluate the relationship between level of PAD, as measured by skin perfusion pressure, and HbA1c using secondary data obtained from charts of patients within the clinic setting. Data included patient gender, age, degree of PAD, and HbA1c. A Pearson's correlation investigated the relationship between the patients' HbA1c and level of PAD. There was a significant relationship between HbA1c and LT PAD (r = .21, p =.009). There was no relation in RT PAD (r =.01, n = 149, p = .90). There was a significant relationship between HbA1c and age (r = .34, p = .00). Ultimately, the goal of this study was to improve PAD recognition, encourage early intervention, and facilitate effective preventive methods. Critical limb ischemia might be delayed or prevented if it is identified earlier by screening methodologies. Early identification and treatment of PAD can improve the quality of life and care for individuals suffering with PAD.

Master of Science / Department of Kinesiology / Steven Copp / Mechanical and metabolic signals arising during skeletal muscle contraction reflexly increase sympathetic nerve activity and blood pressure (i.e., the exercise pressor reflex). In a rat model of simulated peripheral artery disease (PAD) in which a femoral artery is chronically (~72 hours) ligated, the mechanically-sensitive component of the exercise pressor reflex during 1 Hz dynamic contraction is exaggerated compared to that found in normal rats. Whether this is due to an enhanced acute sensitization of mechanoreceptors by metabolites produced during contraction or involves a chronic sensitization of mechanoreceptors is unknown. To investigate this issue, in decerebrate, unanesthetized rats we tested the hypothesis that the increases in mean arterial blood pressure (MAP) and renal sympathetic nerve activity (RSNA) during 1 Hz dynamic stretch are larger when evoked from a previously “ligated” hindlimb compared to those evoked from the contralateral “freely perfused” hindlimb. Dynamic stretch provided a mechanical stimulus in the absence of contraction-induced metabolite production that replicated closely the pattern of the mechanical stimulus present during dynamic contraction. We found that the increases in MAP (freely perfused: 14±1, ligated: 23±3 mmHg, p=0.02) and RSNA were significantly greater during dynamic stretch of the ligated hindlimb compared to the increases during dynamic stretch of the freely perfused hindlimb. These findings suggest that the exaggerated mechanically-sensitive component of the exercise pressor reflex found during dynamic muscle contraction in this rat model of simulated PAD involves a chronic sensitizing effect of ligation on muscle mechanoreceptors and cannot be attributed solely to acute contraction-induced metabolite sensitization.

INTRODUÇÃO: A caminhada é recomendada no tratamento de pacientes com claudicação intermitente (CI) por aumentar a capacidade funcional. Porém, os efeitos cardiovasculares de uma sessão de caminhada foram pouco estudados nestes pacientes. OBJETIVO: Analisar o efeito de uma sessão de caminhada sobre a função e regulação cardiovascular pós-exercício de pacientes com CI. MATERIAS E MÉTODOS: 20 pacientes com CI participaram de duas sessões experimentais realizadas em ordem aleatória: Controle (repouso em pé por 60 minutos) e Exercício (15 séries de dois minutos de caminhada na frequência cardíaca (FC) do limiar de dor, intercaladas por dois minutos de recuperação passiva). Nas duas sessões, a pressão arterial (PA) clínica e de 24 horas, o débito cardíaco (DC - reinalação de CO2), o fluxo sanguíneo para os membros ativo e inativo (plestismografia de oclusão venosa), a capacidade vasodilatadora (hiperemia reativa) e a modulação autonômica cardiovascular (análise espectral da variabilidade da FC e da PA) foram medidas antes e após as intervenções. O volume sistólico (VS) e a resistência vascular (RV) sistêmica foram calculados. Os dados foram analisados pela ANOVA de dois fatores para amostras repetidas, post-hoc de Newman-Keuls e P<0,05. RESULTADOS: O exercício prévio reduziu a PA clínica (PA média = -7±2 mmHg, P<0,05), mas a PA ambulatorial não se modificou. Após o exercício, o VS e o DC diminuíram (-5,62±1,97ml e -0,05±0,13 l/min, P<0,05). A RV sistêmica não se elevou pós-exercício e o exercício prévio impediu o aumento da RV na região ativa e inativa, sem modificar a resposta vasodilatadora. O exercício impediu a redução da FC pós-intervenção, pois impediu o aumento da modulação vagal cardíaca. CONCLUSÃO: Uma única sessão de caminhada promoveu hipotensão pós-exercício (HPE) em pacientes com CI no ambiente clínico, mas este efeito não perdurou no período ambulatorial. A HPE ocorreu pelo efeito do exercício reduzindo o VS e o DC e, simultaneamente, impedindo o aumento da RV sistêmica / INTRODUCTION: Walking exercise (WE) is recommended for patients with intermittent claudication (IC) because it improves functional capacity. However, cardiovascular responses after one session of WE has been poor studied. OBJECTIVE: To analyze the post-effects of a WE session on cardiovascular function and regulation in patients with IC. METHODS: Twenty IC patients randomly underwent two experimental sessions: Control (rest on treadmill for 60 min) and Exercise (fifteen 2-min bouts of WE at the heart rate (HR) of the onset of claudication pain, interpolated with 2-min rest intervals). Before and after the interventions, clinic and ambulatory blood pressure (BP), cardiac output (CO, CO2 rebreathing), blood flow to active and inactive limbs (venous occlusion plethysmography), vasodilatory capacity (reactive hyperemia), cardiovascular autonomic modulation (spectral analysis of HR and BP) were measured in both experimental sessions. Stroke volume (SV) and systemic vascular resistance (VR) were calculated. Data was analyzed by a two-way ANOVA for repeated measures followed by Newman-Keuls post-hoc test, with P<0.05. RESULTS: WE significantly decreased clinic BP ( Mean BP = -7±2 mmHg, P<0.05), but ambulatory BP did not change. After exercise, SV (-5.62±1.97ml) and CO (-0.05±0.13 l/min) decreased (P<0.05), whereas systemic VR did not change. Moreover, previously exercise prevented the increase in VR in the inactive and active limbs without modifying vasodilatory response. Exercise abolished HR decrease after the intervention, because it blunted cardiac vagal modulation increase. CONCLUSION: WE session promoted post-exercise hypotension (PEH) in patients with IC in clinic condition. However, this effect of WE was not maintained during ambulatory period. PEH was promoted by an effect of previous exercise decreasing CO and SV, and simultaneously, preventing an increase in systemic VR

Cardiovascular diseases (CVD) remain the most common cause of death in the United States. Additionally, peripheral artery disease affects thousands of people each year. A major underlying cause of these diseases is the occlusion of the coronary or peripheral arteries due to arteriosclerosis. To overcome this, a number of vascular interventions have been developed including angioplasty, stenting, endarterectomies and bypass grafts. Although all of these methods are capable of restoring blood flow to the distal organ after occlusion, they are all plagued by unacceptably high restenosis rates. While the biological reactions that occur as a result of each of these methods differ, the initiating factor of both the primary atherosclerosis and subsequent failure of vascular interventions appears to be intimal hyperplasia (IH). Intimal hyperplasia is most simply defined as the expansion of multiple layers of cells internally to the internal elastic lamina of the blood vessel. This excessive cellular growth leads to arterial stenosis, plaque formation and inflammatory reactions. Despite extensive research the underlying factors that cause IH remain unclear. A quantity of research to date has implicated endothelial cell mechanosensation as the mechanism by which IH is initiated with evidence positively correlating wall shear stress with IH. Others, however, have demonstrated that changes in the stresses applied to the wall in vitro can modulate IH independent of hemodynamic shear stress. Thus, relations between wall tensile stress and IH in vivo may shed light on the underlying mechanisms of IH. Since noninvasive measurement of wall tensile stress in vivo is difficult, it is most feasible to measure oscillatory wall strain which is intimately related to wall tensile stress through the mechanical properties of the arterial wall. In this dissertation, we hypothesize that reductions in oscillatory wall strain precede the formation of intimal hyperplasia in a murine model. To test our hypothesis, we first developed a novel, high spatial and temporal resolution method to measure oscillatory wall strains in the murine common carotid artery. We validated this method both in vitro using an arterial phantom and in vivo using a murine model of abdominal aortic aneurysms. To assess relationships between strain and IH, we applied our strain measurement technique to a recently developed mouse model of IH. In this model, a suture is used to create a focal stenosis and reduce flow through the common carotid artery by 85%; resulting in proximal IH formation. Using this approach, we identified a relationship between oscillatory strain reductions and IH. Subsequent analysis demonstrated that early reductions in mechanical strain just 4 days after focal stenosis creation correlate with IH formation nearly 1 month later. Since IH is not expected to form by day 4 in this model, we went on to assess changes in gross vascular morphology at day 4. We discovered that, although strains are significantly reduced by day 4, no significant IH can be observed, suggesting that changes in wall structure are resulting in strain reductions. At day 4 post-op, we observed cellular proliferation and leukocyte recruitment to the wall without intimal hyperplasia. These studies suggest that early reductions in mechanical strain may be an important predictor of IH formation. Clinically, this relation could be important for the development of novel techniques for predicting IH formation before it becomes hemodynamically significant.