Toward a new cold and warm nondepolarizing, normokalemic arrest paradigm for orthotopic heart transplantation

Rudd, Donna; Dobson, Geoffrey P.

doi:10.1016/j.jtcvs.2008.06.031

Cited by 20 publications

(30 citation statements)

References 37 publications

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“…Only hearts that met the following predetermined baseline criteria were used in this study: heart rate greater than 200 bpm, regular rhythm, cardiac output greater than 25 mL/min, and coronary flow greater than 10 mL/ min. 22 After the baseline working heart period, hearts were arrested with cardioplegia as described later, and then exposed to ambient room temperature (22 CÀ23 C) for a 60-minute ischemic period. Reperfusion began with retrograde perfusion at 4 mL/min and increased in 0.5-mL/min increments every 30 seconds to 10 mL/min.…”

Section: Isolated Working Heartmentioning

confidence: 99%

Protecting the aged heart during cardiac surgery: Use of del Nido cardioplegia provides superior functional recovery in isolated hearts

Govindapillai

Hua

Rose

et al. 2013

The Journal of Thoracic and Cardiovascular Surgery

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Section: Isolated Working Heartmentioning

confidence: 99%

Protecting the aged heart during cardiac surgery: Use of del Nido cardioplegia provides superior functional recovery in isolated hearts

Govindapillai

Hua

Rose

et al. 2013

The Journal of Thoracic and Cardiovascular Surgery

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“…Nearly 40% of AL (0.1 mM K + ) and 25 mM K + alone hearts failed to return HR, developed pressures or CO after 1 h arrest at 32–33°C. In 2009, Rudd and Dobson advanced the AL cardioplegic concept as a new paradigm for orthotopic heart transplantation, and showed that arrest and reanimation was versatile at both cold (4°C) and warmer (28–30°C) temperatures compared with Celsior solution (Rudd and Dobson, 2009). In 2011, Rudd and Dobson further showed that the rat heart could be placed in suspended animation with AL, insulin and melatonin for 8 h in cold static storage (4°C) and returned 80% of left ventricular function compared to two FDA approved preservation solutions, Custodiol-HTK and Celsior, that could barely return 10% left ventricular function (Rudd and Dobson, 2011b).…”

Section: Adenosine Lidocaine and Mg2+ (Alm™): A More Natural Way Tomentioning

confidence: 99%

Hyperkalemic cardioplegia for adult and pediatric surgery: end of an era?

Dobson¹,

Faggian²,

Onorati³

et al. 2013

Front. Physiol.

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Despite surgical proficiency and innovation driving low mortality rates in cardiac surgery, the disease severity, comorbidity rate, and operative procedural difficulty have increased. Today's cardiac surgery patient is older, has a “sicker” heart and often presents with multiple comorbidities; a scenario that was relatively rare 20 years ago. The global challenge has been to find new ways to make surgery safer for the patient and more predictable for the surgeon. A confounding factor that may influence clinical outcome is high K+ cardioplegia. For over 40 years, potassium depolarization has been linked to transmembrane ionic imbalances, arrhythmias and conduction disturbances, vasoconstriction, coronary spasm, contractile stunning, and low output syndrome. Other than inducing rapid electrochemical arrest, high K+ cardioplegia offers little or no inherent protection to adult or pediatric patients. This review provides a brief history of high K+ cardioplegia, five areas of increasing concern with prolonged membrane K+ depolarization, and the basic science and clinical data underpinning a new normokalemic, “polarizing” cardioplegia comprising adenosine and lidocaine (AL) with magnesium (Mg2+) (ALM™). We argue that improved cardioprotection, better outcomes, faster recoveries and lower healthcare costs are achievable and, despite the early predictions from the stent industry and cardiology, the “cath lab” may not be the place where the new wave of high-risk morbid patients are best served.

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“…Its role in heart preservation is currently being investigated. Results from Dobson et al showed favourable recovery of cardiac parameters after six hours of cold storage in AL solution [67,68].…”

Section: Organ Preservationmentioning

confidence: 99%

Primary Graft Dysfunction After Heart Transplantation

et al. 2014

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Primary graft dysfunction (PGD) is a lifethreatening complication of heart transplantation that presents as left, right, or biventricular dysfunction occurring within the first 24 hours of transplant surgery for which there is no identifiable secondary cause. Myocardial injury caused by acute catecholamine toxicity and the release of multiple proinflammatory mediators in the donor, followed by ischaemiareperfusion injury sustained during retrieval, have been considered the predominant pathogenetic processes leading to PGD. Donor, recipient, and procedural factors contribute to the development and severity of the clinical syndrome. The changing donor and recipient characteristics over the last two decades, particularly the increasing donor and recipient age, have led to heightened risk of PGD. PGD is graded from mild to severe depending on the extent of circulatory support that is required to maintain haemodynamic stability and vital organ function. While advances in acute mechanical support devices have improved the outlook for patients with PGD, the rate of mortality remains high for those with severe PGD, reaching 40 %. Potential approaches to preventing or minimising the severity of PGD include optimising donor management, donor heart preservation, and donor/recipient matching.

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Toward a new cold and warm nondepolarizing, normokalemic arrest paradigm for orthotopic heart transplantation

Cited by 20 publications

References 37 publications

Protecting the aged heart during cardiac surgery: Use of del Nido cardioplegia provides superior functional recovery in isolated hearts

Protecting the aged heart during cardiac surgery: Use of del Nido cardioplegia provides superior functional recovery in isolated hearts

Hyperkalemic cardioplegia for adult and pediatric surgery: end of an era?

Primary Graft Dysfunction After Heart Transplantation

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