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Suleiman MS, Hancock M, Shukla R, et al. Cardioplegic strategies to protect the hypertrophic heart during cardiac surgery. Perfusion. 2011;26:48-56doi: 10.1177/0267659111420607.
Suleiman, M. S., Hancock, M., Shukla, R., Rajakaruna, C., & Angelini, G. D. (2011). Cardioplegic strategies to protect the hypertrophic heart during cardiac surgery. Perfusion, 2648-56. https://doi.org/10.1177/0267659111420607
Suleiman, M-S, et al. "Cardioplegic strategies to protect the hypertrophic heart during cardiac surgery." Perfusion vol. 26 (2011): 48-56. doi: https://doi.org/10.1177/0267659111420607
Suleiman MS, Hancock M, Shukla R, Rajakaruna C, Angelini GD. Cardioplegic strategies to protect the hypertrophic heart during cardiac surgery. Perfusion. 2011 Sep;26:48-56. doi: 10.1177/0267659111420607. PMID: 21933822; PMCID: PMC3272387.
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Perfusion. 2011 Sep;26:48-56. doi: 10.1177/0267659111420607.

Cardioplegic strategies to protect the hypertrophic heart during cardiac surgery.

Perfusion

M-S Suleiman, M Hancock, R Shukla, C Rajakaruna, G D Angelini

Affiliations

  1. Faculty of Medicine & Dentistry, Bristol Heart Institute, University of Bristol, Bristol, UK.

PMID: 21933822 PMCID: PMC3272387 DOI: 10.1177/0267659111420607

Abstract

Cardioplegic arrest and cardiopulmonary bypass are key triggers of myocardial injury during aortic valve surgery. Cardioplegic ischaemic arrest is associated with disruption to metabolic and ionic homeostasis in cardiomyocytes. These changes predispose the heart to reperfusion injury caused by elevated intracellular reactive oxygen species and calcium. Cardiopulmonary bypass is associated with an inflammatory response that can generate systemic oxidative stress which, in turn, provokes further damage to the heart. Techniques of myocardial protection are routinely applied to all hearts, irrespective of their pathology, although different cardiomypathies respond differently to ischaemia and reperfusion injury. In particular, the efficacy of cardioprotective interventions used to protect the hypertrophic heart in patients with aortic valve disease remains controversial. This review will describe key cellular changes in hypertrophy, response to ischaemia and reperfusion and cardioplegic arrest and highlight the importance of optimising cardioprotective strategies to suit hypertrophic hearts.

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