The resuscitation of hearts donated after circulatory death (DCD) is gaining widespread interest; however, the method of initial reperfusion (IR) that optimizes functional recovery has not been elucidated. We sought to determine the impact of IR temperature on the recovery of myocardial function during ex vivo heart perfusion (EVHP). Eighteen pigs were anesthetized, mechanical ventilation was discontinued, and cardiac arrest ensued. A 15-min standoff period was observed and then hearts were reperfused for 3 min at three different temperatures (5°C; N = 6, 25°C; N = 5, and 35°C; N = 7) with a normokalemic adenosine-lidocaine crystalloid cardioplegia. Hearts then underwent normothermic EVHP for 6 h during which time myocardial function was assessed in a working mode. We found that IR coronary blood flow differed among treatment groups (5°C = 483 ± 53, 25°C = 722 ± 60, 35°C = 906 ± 36 mL/min, p < 0.01). During subsequent EVHP, less myocardial injury (troponin I: 5°C = 91 ± 6, 25°C = 64 ± 16, 35°C = 57 ± 7 pg/mL/g, p = 0.04) and greater preservation of endothelial cell integrity (electron microscopy injury score: 5°C = 3.2 ± 0.5, 25°C = 1.8 ± 0.2, 35°C = 1.7 ± 0.3, p = 0.01) were evident in hearts initially reperfused at warmer temperatures. IR under profoundly hypothermic conditions impaired the recovery of myocardial function (cardiac index: 5°C = 3.9 ± 0.8, 25°C = 6.2 ± 0.4, 35°C = 6.5 ± 0.6 mL/minute/g, p = 0.03) during EVHP. We conclude that the avoidance of profound hypothermia during IR minimizes injury and improves the functional recovery of DCD hearts.
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http://dx.doi.org/10.1111/ajt.13574 | DOI Listing |
Acute myocardial infarction (MI) is a leading cause of death worldwide. Although with current treatment, acute mortality from MI is low, the damage and remodeling associated with MI are responsible for subsequent heart failure. Reducing cell death associated with acute MI would decrease the mortality associated with heart failure.
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December 2024
Department of cardiology, Guy's and St Thomas' NHS Foundation Trust, Harefield Hospital, London, UK; King's College London, London, UK.
Background: ST-segment elevation myocardial infarction (STEMI) is treated with immediate primary percutaneous coronary intervention (pPCI) to restore coronary blood flow in the acutely ischaemic territory, but is associated with reperfusion injury limiting the benefit of the therapy. No treatment has proven effective in reducing reperfusion injury. Transcoronary hypothermia has been tested in clinical studies and is well tolerated, but is generally established after crossing the occlusion with a guidewire therefore after initial reperfusion, which might have contributed to the neutral outcomes.
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December 2024
Department of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
The innate immune response is the body's first line of defense against external pathogens and endogenous damage signals. The cGAS-STING pathway is a crucial component of the innate immune response, playing a key role in initiating antiviral and anti-infective immune responses by recognizing cytosolic DNA. Acute cerebral infarction is one of the leading causes of death and disability worldwide, with the primary treatment approach being the restoration of blood flow to ischemic brain tissue.
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Heart Centre Leipzig, University Clinic of Cardiac Surgery, HELIOS Clinic, University Leipzig, Leipzig, Germany.
Objective: Myocardial protection is important for a successful procedure cardiac surgery, and the key element of myocardial protection is cardioplegia. We compared Del Nido cardioplegia (DN) and Bretschneider histidine-tryptophan-ketoglutarate cardioplegia (HTK) regarding cardioprotective effects in a porcine model of prolonged ischaemia.
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Inflammation
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Department of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Microglia, the central nervous system's primary immune cells, play a key role in the progression of cerebral ischemic stroke, particularly through their involvement in pyroptosis. The long non-coding RNA taurine up-regulated gene 1 (Tug1) is elevated during ischemic stroke and is critical in driving post-stroke neuroinflammation. However, the underlying molecular mechanisms remain unclear.
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