Describing current use, barriers, and facilitators of patient portal messaging for research recruitment: Perspectives from study teams and patients at one institution.

Introduction: The electronic health record (EHR) and patient portal are used increasingly for clinical research, including patient portal recruitment messaging (PPRM). Use of PPRM has grown rapidly; however, best practices are still developing. In this study, we examined the use of PPRM at our institution and conducted qualitative interviews among study teams and patients to understand experiences and preferences for PPRM. Methods: We identified study teams that sent PPRMs and patients that received PPRMs in a 60-day period. We characterized these studies and patients, in addition to the patients' interactions with the PPRMs (e.g., viewed, responded). From these groups, we recruited study team members and patients for semi-structured interviews. A pragmatic qualitative inquiry framework was used by interviewers. Interviews were audio-recorded and analyzed using a rapid qualitative analysis exploratory approach. Results: Across ten studies, 35,037 PPRMs were sent, 33% were viewed, and 17% were responded to. Interaction rates varied across demographic groups. Six study team members completed interviews and described PPRM as an efficient and helpful recruitment method. Twenty-eight patients completed interviews. They were supportive of receiving PPRMs, particularly when the PPRM was relevant to their health. Patients indicated that providing more information in the PPRM would be helpful, in addition to options to set personalized preferences. Conclusions: PPRM is an efficient recruitment method for study teams and is acceptable to patients. Engagement with PPRMs varies across demographic groups, which should be considered during recruitment planning. Additional research is needed to evaluate and implement recommended changes by study teams and patients.

Femoral artery diameter and arteriogenic cytokines in healthy women.

Animal studies have identified monocyte chemoattractive protein-1 (MCP-1) and vascular endothelial growth factor (VEGF) as critical mediators of arterial diameter enlargement in response to chronic increases in blood flow (arteriogenesis). Furthermore, cellular studies have shown that the shear stresses resulting from increased blood flow stimulate synthesis of MCP-1, which in turn stimulates synthesis of VEGF. The purpose of this study was to determine if these mechanisms are evident in healthy women. Resting femoral artery diameter and blood flow, lean leg mass, MCP-1 and VEGF concentrations, and aerobic capacity were measured in 34 healthy women along with plasma concentrations of lipids associated with cardiovascular disease risk. Femoral artery diameter was independently related to metabolically active (lean) leg mass (b=0.41, P=0.008) and aerobic capacity (b=0.45, P=0.004). Plasma MCP-1 correlated negatively with the ratio of femoral artery diameter to lean leg mass (b=-0.42, P=0.009) and positively with serum triglycerides (b=0.46, P=0.005). Plasma VEGF exhibited similar correlations and strongly correlated with MCP-1 (R=0.92, P<0.0001). The results indicate that circulating MCP-1 and VEGF concentrations are associated with both arteriogenic and atherogenic stimuli in healthy women.

Femoral artery remodeling after aerobic exercise training without weight loss in women.

BACKGROUND: It is currently unclear whether reductions in adiposity mediate the improvements in vascular health that occur with aerobic exercise. The purpose of this longitudinal study of 13 healthy women (33 +/- 4 years old) was to determine whether 14 weeks of aerobic exercise would alter functional measures of vascular health, namely resting aortic pulse wave velocity (aPWV, an index of arterial stiffness), femoral artery diameter (D(FA)), and femoral artery blood flow (BF(FA)) independent of changes in adiposity. METHODS: Aerobic fitness was assessed as VO2peak normalized to fat-free mass, and adiposity (percent body fat) was determined by dual energy x-ray absorptiometry. Serum concentrations of proteins associated with risk for cardiovascular disease, including C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and leptin, were also measured. Subjects cycled for 50 minutes, 3 times per week. RESULTS: Aerobic fitness normalized to fat-free mass increased 6% (P = 0.03) whereas adiposity did not change. Resting D(FA) increased 12% (P < 0.001) and resting shear rate decreased 28% (P = 0.007). Aortic PWV, and serum sICAM-1, CRP and leptin did not change with training. CONCLUSION: Significant reductions in adiposity were not necessary for aerobic exercise training to bring about improvements in aerobic fitness and arterial remodeling. Peripheral arterial remodeling occurred without changes in central arterial stiffness or markers of inflammation.

Leptin, blood pressure, and aerobic capacity in women.

BACKGROUND: In animals, the adipocyte-derived hormone leptin induces increased blood pressure centrally via the hypothalamus, and one study has reported that exercise training decreases hypothalamic leptin receptor expression. In humans, high circulating leptin concentrations are associated with high blood pressure, but the possible influence of physical activity or aerobic capacity on this association is unknown. METHODS: Forty-two healthy women, 25-40 years of age, with diverse ranges of body fatness and aerobic capacities, were studied under basal resting conditions. Blood pressure (sphygmomanometry), arterial stiffness (pulse wave velocity (PWV)), percent body fat (dual energy X-ray absorptiometry), circulating concentrations of leptin, soluble leptin receptor (sLR) (enzyme-linked immunoassay), and nitric oxide (Griess reaction) were measured. RESULTS: Serum leptin correlated with percent body fat (R(2) = 0.74, P < 0.0001) but was not significantly associated with aerobic capacity. Blood pressure correlated positively with serum leptin concentrations and had a negative interaction with aerobic capacity for both systolic (overall model: R(2) = 0.33, P = 0.002) and diastolic (R(2) = 0.48, P < 0.0001) pressure. The relation between leptin and blood pressure was attributable solely to women with below-median aerobic capacity even though their body fat percentages and leptin concentrations were similar to those of women above the median. The results could not be attributed to differences in peripheral factors such as sLR or nitric oxide concentrations or to differences in arterial stiffness determined by aortic PWV. CONCLUSIONS: Circulating leptin concentrations are related to body fatness, but the hypertensive influence of leptin is modified by physical fitness.