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Abstract Details

Polygenic Susceptibility to Hypertension is Associated with Uncontrolled and Resistant Hypertension in Stroke Survivors
Cerebrovascular Disease and Interventional Neurology
Cerebrovascular Disease and Interventional Neurology Posters (7:00 AM-5:00 PM)
217
To test the hypothesis that polygenic susceptibility to hypertension (PSH) leads to higher blood pressure (BP) and increased risk of uncontrolled hypertension (UHTN) and resistant hypertension (RHTN) in stroke survivors.
Blood pressure is a highly heritable trait with numerous related genetic risk variants identified. While prior studies showed that PSH is associated with elevated BP, UHTN, RHTN and risk of stroke, its role after a cerebrovascular event remains unknown.
We conducted a nested study within the UK Biobank, including individuals of European ancestry with a prevalent ischemic or hemorrhagic stroke. To model PSH, we created polygenic risk scores (PRS) for systolic, diastolic and pulse BP using 732 previously discovered loci. We divided the PRS into quintiles and used linear and logistic regression to test whether higher PSH led to higher observed BP as well as increased risk of UHTN (SBP >140 mmHg or DBP >90 mmHg) and RHTN (UHTN despite being on >=3 antihypertensive drugs) in stroke survivors.
Of the 502,536 participants enrolled in the UK Biobank, 5,815 (1.2%) with a prevalent stroke at enrollment were included. We found the following results across quintiles 1 through 5 of the systolic BP-based PRS: mean systolic BP 138.4, 140.6, 141.8, 142.9 and 145.8 mmHg (unadjusted p<0.0001); risk of UHTN 46%, 51%, 52%, 56% and 59% (unadjusted p<0.0001); and risk of RHTN 1.9%, 3.8%, 4.7%, 5.8% and 6.7% (unadjusted p<0.0001). We obtained similar results when both evaluating diastolic and pulse BP-based PRSs and using multivariable models adjusted by sex, age and genetic principal components (all p<0.0001).
PSH is associated with observed BP and risk of UHTN and RHTN in stroke survivors. Follow up research should evaluate whether precision medicine strategies based on BP-related genetic information can help identify patients that could benefit from aggressive diagnostic and/or therapeutic interventions.
Authors/Disclosures

PRESENTER 		No disclosure on file
No disclosure on file
Natalia Szejko, MD, PhD Dr. Szejko has nothing to disclose.
Stacy C. Brown, MD (The Queen's Medical Center, Neuroscience Institute) Dr. Brown has nothing to disclose.
Nils Petersen, MD, FÂ鶹´«Ã½Ó³»­ (Yale University) The institution of Dr. Petersen has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for Silkroad Medical. Dr. Petersen has received research support from NIH.
Lauren H. Sansing, MD Dr. Sansing has nothing to disclose.
Kevin N. Sheth, MD, FÂ鶹´«Ã½Ó³»­ (Yale UniversityDivision of Neuro and Critical Care) Dr. Sheth has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Ceribell. Dr. Sheth has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Zoll. Dr. Sheth has received personal compensation in the range of $10,000-$49,999 for serving on a Scientific Advisory or Data Safety Monitoring board for NControl. Dr. Sheth has received stock or an ownership interest from Astrocyte. Dr. Sheth has received stock or an ownership interest from Alva. The institution of Dr. Sheth has received research support from Biogen. The institution of Dr. Sheth has received research support from Novartis. The institution of Dr. Sheth has received research support from Bard. The institution of Dr. Sheth has received research support from Hyperfine. Dr. Sheth has received intellectual property interests from a discovery or technology relating to health care.
Guido J. Falcone, MD (Yale School of Medicine) The institution of Dr. Falcone has received research support from NIH. The institution of Dr. Falcone has received research support from AHA.