scholarly journals APOL1 genotype, blood pressure, and survival in African Americans with nondiabetic nephropathy

2017 ◽  
Vol 91 (2) ◽  
pp. 276-278 ◽  
Author(s):  
Todd W. Robinson ◽  
Barry I. Freedman
2010 ◽  
Vol 24 (2) ◽  
pp. 199-208 ◽  
Author(s):  
Elizabeth C. Leritz ◽  
David H. Salat ◽  
William P. Milberg ◽  
Victoria J. Williams ◽  
Caroline E. Chapman ◽  
...  

2009 ◽  
Vol 11 (12) ◽  
pp. 720-725 ◽  
Author(s):  
Nadya Merchant ◽  
Charles D. Searles ◽  
Anbu Pandian ◽  
Syed T. Rahman ◽  
Keith C. Ferdinand ◽  
...  

1999 ◽  
Vol 99 (11) ◽  
pp. 1380-1391 ◽  
Author(s):  
SHIRIKI K KUMANYIKA ◽  
LUCILE ADAMS-CAMPBELL ◽  
BARBARA VAN HORN ◽  
THOMAS R TEN HAVE ◽  
JUDITH A TREU ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Mildred A. Pointer ◽  
Sadiqa Yancey ◽  
Ranim Abou-Chacra ◽  
Patricia Petrusi ◽  
Sandra J. Waters ◽  
...  

Although several studies have shown that enhanced cardiovascular reactivity can predict hypertension development in African Americans, these findings have not been consistent among all studies examining reactivity and hypertension susceptibility. This inconsistency may be explained by the influence of anxiety (state and trait) on the blood pressure response to stress. Therefore, this study sought to determine whether anxiety is associated with blood pressure response to cold pressor (CP) and anger recall (AR) stress tests in young healthy African Americans. Modeling using state and trait anxiety revealed that state anxiety predicts systolic (SBP) and diastolic blood pressure DBP response to CP and AR (P≤0.02). Interestingly, state anxiety predicted heart rate changes only to CP (P<0.01;P=0.3for AR). Although trait anxiety was associated with SBP response to AR and not CP, it was not a significant predictor of reactivity in our models. We conclude that anxiety levels may contribute to the variable blood pressure response to acute stressors and, therefore, should be assessed when performing cardiovascular reactivity measures.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Kobina A Wilmot ◽  
Ibhar Al Mheid ◽  
Ronnie Ramadan ◽  
Pratik M Pimple ◽  
Amit J Shah ◽  
...  

Introduction: Increased hemodynamic responses to psychological stress have been associated with adverse CAD events. African Americans (AA) have worse CAD outcomes than other groups. Heightened hemodynamic responses to stress may play a role. Our hypothesis was that AA would have higher hemodynamic reactivity to a standardized mental stress compared to Non-African Americans (NAA). Methods: We evaluated 574 patients (163 AA) with CAD, who underwent a standardized mental stress challenge. Hemodynamics were obtained at rest, during stress (speaking task), and during recovery. The rate-pressure product (RPP) was calculated as systolic blood pressure (SBP) x heart rate (HR). Hemodynamic reactivity was evaluated as the difference in RPP at rest and during stress. Depressive symptoms were measured with the Beck Depression Inventory-II (BDI). Results: As compared to NAA, AA patients were younger, had lower education and income, and higher prevalence of diabetes, obesity, hypertension, smoking, and depressive symptoms (BDI mean scores 9.8 vs. 7.6, p= 0.003). AA patients had higher blood pressure during all three periods (Table). However, hemodynamic reactivity with stress was significantly lower in AA than NAA (RPP reactivity 3114 vs 3620, p= 0.02). Adjusting for baseline RPP, age, gender and smoking did not substantially alter the association. However, after adjusting for depressive symptoms, the association was attenuated by 23% (p=0.16). BMI, diabetes and beta-blocker use had minimal additional explanatory role. In the final model, baseline RPP, depressive symptoms and BMI were significantly associated with a lower RPP reactivity (p<0.01). Conclusion: AA patients with CAD, compared with NAA, have elevated blood pressure throughout mental stress, but tend to have blunted hemodynamic reactivity to stress. Depressive symptoms, which are more elevated among AA, play a role in this different response to stress and may be implicated in the higher CAD risk of this group.


2019 ◽  
Vol 101 ◽  
pp. 19-26 ◽  
Author(s):  
Jacqueline Woerner ◽  
Todd Lucas ◽  
Jennifer Pierce ◽  
Jenna L. Riis ◽  
Douglas A. Granger

2000 ◽  
Vol 6 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Mary Bondmass ◽  
Nadine Bolger ◽  
Gerard Castro ◽  
Boaz Avitall

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