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Brain death effects on catecholamine levels and subsequent cardiac damage assessed in organ donors
Silvia Pérez López1, Jesús Otero Hernández, Natalia Vázquez Moreno
1Unidad de Coordinación de Trasplantes y Terapia Celular, Hospital Universitario Central de Asturias, Oviedo, Spain. silvia.perez@sespa.princast.es
Insights
Brain death (BD) causes cardiac lesions and hormone surges. This study found significant catecholamine increases and myocardial damage in BD donors, impacting heart transplant viability.
Area of Science:
- Cardiology
- Transplantation Immunology
- Neuroendocrinology
Background:
- Brain death (BD) induces hemodynamic and neuroendocrine changes, including a catecholamine surge.
- This surge can cause cardiac histologic lesions (contraction bands, mononuclear cell infiltrates, cardiomyocyte necrosis).
- These BD-associated cardiac changes may impair heart function and affect transplant outcomes.
Purpose of the Study:
- To investigate the catecholamine surge and release patterns in brain death (BD) donors.
- To examine the prevalence and characteristics of cardiac histologic lesions in hearts from BD donors.
- To assess the potential impact of BD on cardiac graft quality for transplantation.
Main Methods:
- Histologic examination of left ventricle specimens from 50 BD donors.
- Measurement of catecholamine levels (epinephrine, norepinephrine, dopamine) via HPLC in arterial blood samples from 40 BD donors at multiple time points.
- Analysis of catecholamine surge timing and magnitude, and correlation with observed cardiac lesions.
Main Results:
- Elevated levels of epinephrine (2.36-fold), norepinephrine (8.56-fold), and dopamine (54.76-fold) were observed.
- Catecholamine release patterns showed peaks for epinephrine and dopamine at BD diagnosis, and norepinephrine 1 hour post-BD.
- Cardiac lesions included contraction bands (50%), cardiomyocyte necrosis (62%), focal mononuclear cell infiltrates (18%), and apoptotic damage (40%).
Conclusions:
- Brain death is associated with significant cardiac lesions, including apoptotic damage in over 50% of donors.
- Observed catecholamine surges were generally lower than previously reported, except for dopamine.
- The findings highlight the heterogeneity of BD-associated cardiac pathology and its potential implications for heart transplantation.
Background:
Brain death (BD) causes hemodynamic and neuroendocrine alterations including a catecholamine surge, which in turn causes histologic lesions in cardiac muscle such as contraction bands, focal mononuclear cell infiltrates and cardiomyocyte necrosis. These changes are likely to compromise heart function and could therefore also affect the graft response after heart transplantation. This study was designed to examine the catecholamine surge, the catecholamine release pattern and the histologic lesions traditionally described as characteristic of BD in hearts procured from BD donors.
Methods:
After BD diagnosis, specimens were taken from the left ventricle (n = 50) for histologic examination. Arterial blood samples were collected from 40 of the donors at different time-points (1 hour before BD; on BD diagnosis; and 1, 2, 3 and 4 hours after BD) to determine catecholamine levels by high-performance liquid chromatography (HPLC).
Results:
The three hormones examined showed above-normal levels (epinephrine 2.36-fold, norepinephrine 8.56-fold, dopamine 54.76-fold). Release patterns included epinephrine and dopamine peaks at the time of BD and a norepinephrine peak 1 hour later. Fifty percent of the BD donors showed contraction bands and 62% displayed cardiomyocyte necrosis, which was associated with focal mononuclear cell infiltrates in 18% of cases. In 40% of donors, colocalized apoptotic and necrotic damage was observed.
Conclusions:
Differing extents of BD-associated cardiac lesions were observed in the donors, and >50% also showed apoptotic damage. The expected catecholamine peak at the time of BD was only detected for epinephrine and dopamine. Hormone increases were below those described in the literature, except for dopamine.
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