Cardioplegia in aortic stenosis must protect a ventricle altered by chronic pressure overload, increased muscle mass, fibrosis, and impaired coronary perfusion reserve. A focused review by Ho and colleagues examines how these changes affect myocardial protection during surgical aortic valve replacement (AVR). Its central finding is that no cardioplegic formulation, temperature, or delivery route has demonstrated consistent superiority in clinically important outcomes.
What Was Reviewed?
The authors searched PubMed, Embase, and the Cochrane Library, updating their searches in July 2026. They prioritized comparative human studies involving aortic stenosis or AVR, while drawing on mixed cardiac surgery populations, other valve procedures, and experimental research when direct evidence was unavailable.
This is a focused narrative review. It did not use formal eligibility criteria, protocol registration, a structured risk-of-bias assessment, or a meta-analysis. The synthesis helps explain clinical uncertainties, but it does not provide pooled estimates of benefit or establish a preferred protocol.
Why the Hypertrophied Ventricle Matters
Left ventricular hypertrophy increases the amount of myocardium requiring protection. Microvascular growth may not keep pace with muscle mass, while fibrosis and impaired relaxation further compromise perfusion reserve. Two patients with similar valve gradients can therefore have very different myocardial protection requirements.
The review also distinguishes the physiology of the beating heart from cardioplegic arrest. Bypass decompression and electromechanical arrest remove much of the dynamic compression affecting coronary flow, but increased muscle mass, fibrosis, and microvascular abnormalities remain. Measurements of coronary reserve help explain vulnerability; they do not directly determine cardioplegia flow or dose during arrest.
Cardioplegia in Aortic Stenosis: What the Comparisons Show
| Evidence summarized in the review | Main finding | Interpretive limit |
|---|---|---|
| Cold versus warm blood cardioplegia; randomized study of 35 patients with AS-related hypertrophy | Cold delivery was associated with less metabolic stress and lower troponin I release. | Small study centered on biochemical outcomes. |
| Cold blood versus cold crystalloid; randomized study of 80 isolated-AS patients | Peak CK-MB and troponin T were approximately twice as high with crystalloid. | The trial could not establish differences in major clinical outcomes. |
| Custodiol/HTK versus cold Calafiore blood; 7,263 AVR procedures with 825 matched pairs | Operative mortality, complications, and long-term survival were similar. | Retrospective data covering mixed valve pathology and substantial changes in practice over time. |
| Buckberg versus del Nido; two-center randomized trial of 311 adults undergoing isolated AVR | Biomarker release was similar; del Nido produced more spontaneous rhythm recovery and less ventricular fibrillation requiring defibrillation. | Included stenosis, regurgitation, and mixed disease; results were not stratified by LV mass. |
These are selected studies discussed by the authors, rather than a pooled analysis. Differences in temperature, delivery route, redosing, patient selection, and operative complexity make simple comparisons by solution name unreliable.
Temperature and Composition Cannot Always Be Separated
A study comparing cold crystalloid with warm blood changes two variables at once. A lower enzyme release in one group cannot identify whether temperature, composition, or their interaction produced the difference. Similarly, a terminal warm reperfusion dose or “hot shot” is a separate intervention from warm maintenance cardioplegia throughout cross-clamping.
Dose, Delivery, and Redosing
Body-weight-based dosing is convenient, but it may poorly reflect the myocardial mass of a markedly hypertrophied ventricle. A historical study of 28 patients linked higher initial cold crystalloid volume per gram of LV mass with less postoperative enzyme release. No validated contemporary LV-mass-based dosing regimen exists. The historical numerical threshold should not be transferred to modern blood, del Nido, or HTK protocols.
Increasing crystalloid volume also carries systemic consequences, including hemodilution and electrolyte or acid-base disturbances. The review specifically discusses acute iso-osmotic hyponatremia with low-sodium HTK. Adequate myocardial exposure and the effects of the administered volume must be assessed together.
Antegrade delivery may use the aortic root or direct coronary ostial administration. Significant aortic regurgitation can compromise root delivery and allow LV distension. Retrograde delivery can supplement protection when coronary disease, difficult ostial access, or concern about maldistribution is present, but retrograde-only administration may incompletely perfuse the right ventricle. The available AS-specific evidence does not establish routine superiority of a retrograde strategy.
Prolonged-action solutions can reduce operative interruptions, but the initial dose does not remove the need to plan for unexpectedly long cross-clamping. Myocardial temperature, persistence of arrest, recurrent electrical activity, delivery conditions, and elapsed time all contribute to assessing protection. A low regional temperature alone cannot confirm adequate dose or uniform distribution.
Relevance for Perfusion Teams
The review supports evaluating the full myocardial protection protocol: composition and blood-to-crystalloid ratio, initial volume and indexing method, infusion pressure and duration, temperature, route, redosing plan, terminal reperfusion, and total cross-clamp time. Preoperative LV mass and function, associated regurgitation or coronary disease, and expected procedural complexity provide essential context.
For quality improvement, postoperative troponin and CK-MB should be interpreted alongside rhythm recovery, defibrillation, inotropic support, low-cardiac-output syndrome, mechanical support, renal injury, and ventricular function. Biomarker release is a useful signal, but it is neither specific for cardioplegia failure nor a substitute for patient-centered outcomes.
Limitations and Disclosures
The evidence specific to severe AS is limited, often historical, and frequently based on small studies using surrogate outcomes. Larger cohorts introduce treatment-selection and institutional confounding, while mixed AVR populations may not reflect marked AS-related hypertrophy. Because this review lacks a systematic risk-of-bias assessment or quantitative synthesis, its conclusions should guide critical appraisal rather than be treated as definitive solution-specific recommendations.
The authors call for prospective multicenter studies stratified by LV mass, ventricular function, and cross-clamp duration, with standardized reporting of complete protocols and clinically meaningful outcomes. They reported no external funding and no conflicts of interest.
Original Article
Ho M, Chapman B, Lucchese G, Bosco P. Cardioplegia Strategies in Aortic Stenosis: A Focused Review of Current Evidence for Surgical Considerations. Reviews in Cardiovascular Medicine. 2026;27(10):52775. doi:10.31083/RCM52775.
The original article is available under a Creative Commons Attribution 4.0 license. The linked source PDF is unchanged. The cover is an AI-generated conceptual editorial image.
