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Singh et al. Myocardial protection in cardiac transplantation

Allopurinol with glutathione act as antioxidants [40,41] . UW BIOMARKERS
limited ischaemic damage from prolonged storage and
improved myocardial function in the early posttransplant Cardiac troponins have largely replaced cardiac muscle
period, thus allowing transplantation of organs with enzymes (CK-MB) for the diagnosis of myocardial
ischaemic times > 300 min [42] . Jeevanandam et al. [43] infarction. Cardiac troponin T (cTnT) and troponin I (cTnI)
performed a study comparing University of Wisconsin are cardiac regulatory proteins that control the calcium
solution with crystalloid cardioplegia to saline storage mediated interaction between actin and myosin. cTnT
and noted a significant improvement in mean time is also expressed in small amounts in skeletal muscles
from reperfusion to achieving a stable rhythm, need for as well. The role of post-operative troponin release as
intraoperative defibrillation, need for cardiac pacing and a prognostic factor for mid- and short-term all-cause
CK-MB release over 48 h. They however also reported mortality after adult cardiac surgery is accepted albeit
higher CK-MB levels (335 IU) post-operatively despite cut-off values are difficult to establish due to the variety
a relatively shorter ischaemic time of 153 min when of timing of the Tn testing, Tn subunit and Tn assays [59] .
compared to the HTK group of Minami’s cohort [26] . Its prognostic value in a transplant setting however
has not been clearly understood. CK-MB and troponin
Celsior I are released immediately after transplantation and
Dr Menasche and colleagues developed Celsior depends on myocardial ischaemic damage, which is
solution [44] . They utilised lactobionate and mannitol as related to ischaemic time [60] .
impermeants. Celsior also uses histidine as a buffer
and glutamate as an energy substance alongside De Santo et al. [60] investigated troponin release after
magnesium to stabilise calcium levels. Unlike UW cardiac transplantation. Data from 362 consecutive
which has a high potassium content, Celsior had recipients were collated over 11 years. Target outcomes
a lower potassium content and a high sodium included factors determining troponin release, early
concentration. In canine models, Celsior had a similar graft failure, rise in creatinine and operative death.
cardioprotective profile as UW. Higher concentrations This study depicted the largest group of adult cardiac
of potassium results in increase coronary vascular transplantation patients who had cTnI levels correlated
resistance secondary to endothelial distension [45,46] . De with perioperative morbidity and mortality reported in
Santo et al. compared the results of “high risk” grafts the literature thus far. The pattern of troponin release
[46]
vs. “standard” grafts using Celsior. They followed up observed was similar to that reported by Minami.
200 consecutive heart recipients with 73 in the high- cTnI release > 10 μg/L proved to be an independent
risk group (defined as 2 or more of the following: age predictor for early graft dysfunction which in turn
> 45, female, high pre-retrieval inotropic support, size was a determinant of hospital mortality. Factors that
mismatch > 20%, and ischaemia time > 180 min) and predicted this rise included previous cardiac surgery,
127 in the standard group. There was no difference left ventricular hypertrophy, increased ischaemic
time and transplant status 2B. Troponin proteins are
noted between the two groups in terms of 1-year intracellular proteins released primarily from cardiac
mortality, hospital mortality, histological findings and myocytes undergoing cellular necrosis. Perhaps
patterns of enzyme release [47] .
surprisingly, ischaemia/reperfusion injury following
cardiac transplantation may not cause cellular necrosis
Comparison of cardioplegic solutions and occasionally troponin concentrations may not be
Lee et al. [48] combined both the intracellular and increased [61] .
extracellular cardioplegic solutions (HTK and StH).
In their cohort of 31 patients, they demonstrated non- Brain natriuretic peptide (BNP) is actively synthesized
inferiority to other approaches. The theoretical benefits and released from cardiac myocytes in response
include the quick initial arrest from StH alongside to ischaemia and inflammation [62] . It is not directly
the prolonged effect of HTK alongside its buffering stimulated by surgical manipulation or cardiopulmonary
mechanism. The effectiveness of HTK has resulted bypass, hence its role as a biomarker for ischaemic
in lower CK and lactate dehydrogenase levels in non- reperfusion injury in non-transplant cardiac surgery to
transplant cardiac surgery [Table 2] [48,49] . predict post-operative dysfunction [63,64] . McIlroy et al. [65]
studied the role of BNP as marker for myocardial
Comparisons between the different crystalloid ischaemic reperfusion in 25 consecutive patients
cardioplegia solutions are difficult to extrapolate due to following cardiac transplantation. The median
the lack of direct comparisons. Several smaller animal preoperative troponin-I concentrations were almost
studies however do suggest potential superiority of three-fold the upper limit of normal in both the donor
HTK cardioplegia over the rest. and recipient. The donor BNP levels centred around

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