ArticleJTCVS open2026
Uncontrolled hypertension contributes to vascular permeability after cardioplegic arrest and cardiopulmonary bypass.
Article in JTCVS open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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10 authors.
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Abstract
Objective: Vasoplegia and endothelial dysfunction are well-known complications of cardioplegia and cardiopulmonary bypass (CP/CPB). Our lab has previously shown that endothelial adherens junction impairment is driven by vascular endothelial (VE)-cadherin phosphorylation. In this study we investigate the interplay of hypertension and CP/CPB. Methods: Right atrial tissue was harvested pre- and post-CP/CPB from patients undergoing surgery. Patients were stratified into nonhypertensive, controlled hypertension, and uncontrolled hypertension groups based on history and in-office blood pressure measurements. Atrial tissue was sent for transcriptomics. Expression, phosphorylation, and localization of VE-cadherin was assessed by immunoblotting and immunohistochemistry. Atrial microvascular reactivity to adenosine diphosphate was assessed by videomicroscopy. Results: Several genes related to reactive oxygen species handling, nitric oxide signaling, and adherens junctions were suppressed in patients with uncontrolled hypertension versus nonhypertensive patients pre-CP/CPB. By immunoblotting, patients with uncontrolled hypertension had significantly higher levels of phosphorylated VE-cadherin (p-VE cadherin) and higher ratios of p-VE cadherin/VE-cadherin compared with nonhypertensive ( Conclusions: Our study supports a 2-hit model in which hypertension primes the endothelium for dysfunction, and CP/CPB amplifies this injury through impaired reactive oxygen species handling, nitric oxide dysregulation, and adherens junction destabilization. These findings highlight the importance of preoperative hypertension management to improve postoperative outcomes.
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