Key result
Cold blood cardioplegia reduces biomarker release in severe aortic stenosis, but shows no clinical superiority.
Why the study?
Myocardial hypertrophy, fibrosis, and microvascular dysfunction in severe AS increase susceptibility to ischemic injury and complicate homogeneous cardioplegic delivery during surgical AVR, while AS-specific comparative studies on cardioplegia remain limited.
Does any specific cardioplegia strategy (composition, temperature, delivery route, or dosing) improve myocardial protection and clinical outcomes in adults with severe aortic stenosis undergoing surgical aortic valve replacement?
Does any specific cardioplegia strategy (composition, temperature, delivery route, or dosing) improve myocardial protection and clinical outcomes in adults with severe aortic stenosis undergoing surgical aortic valve replacement?
In adults with severe aortic stenosis undergoing surgical aortic valve replacement, no single cardioplegia formulation, temperature, or delivery route has demonstrated consistent superiority in clinical outcomes, necessitating individualized myocardial protection protocols that account for left ventricular hypertrophy and anticipated cross-clamp duration.
Answers are grounded in this paper and cite their sources.
No cardioplegia strategy shows clinical superiority in severe aortic stenosis; leaves open hypertrophy-adjusted dosing trials before practice change.
Severe aortic stenosis (AS) exposes the hypertrophied myocardium to cardioplegic arrest in the setting of increased left ventricle (LV) mass, interstitial fibrosis, impaired relaxation, coronary microvascular dysfunction, and reduced perfusion reserve. These abnormalities may increase susceptibility to ischemic injury and complicate homogeneous cardioplegic delivery. This focused narrative review synthesizes physiological and clinical evidence on cardioplegia composition, temperature, delivery route, dosing, redosing, and myocardial protection during prolonged aortic cross-clamping in adults undergoing surgical aortic valve replacement. AS-specific comparative studies remain limited, generally small, and frequently reliant on biochemical markers; meanwhile, larger observational cohorts and contemporary randomized aortic valve replacement (AVR) trials also vary substantially in patient selection and myocardial protection protocols. Although some studies have associated cold blood cardioplegia with lower biomarker release than cold crystalloid cardioplegia, and cold maintenance strategies with less biochemical injury than warm cardioplegia, no formulation, temperature, or delivery route has demonstrated consistent superiority in clinically important outcomes. Limited historical evidence also suggests that body weight-based dosing may inadequately reflect myocardial requirements in marked LV hypertrophy, but no validated LV mass-based regimen currently exists. Therefore, cardioplegia in severe AS should be considered within a comprehensive myocardial protection protocol incorporating composition, temperature, dose, delivery route, redosing strategy, myocardial phenotype, associated valve or coronary disease, and anticipated cross-clamp duration. Prospective AS-specific studies using standardized protocols, LV mass stratification, and clinically meaningful outcomes are required.
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Ho et al. (2026) conducted a review in Severe aortic stenosis undergoing surgical aortic valve replacement. Cardioplegic myocardial protection strategies (e.g., cold/warm blood, crystalloid, Del Nido, Custodiol/HTK) vs. Alternative cardioplegia formulations, temperatures, dosing regimens, or delivery routes was evaluated. Cardioplegia strategies in severe aortic stenosis show lower biomarker release with cold blood protocols, but no formulation, temperature, or route demonstrates consistent clinical superiority.
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