Cold versus Warm Cardioplegia 
The cardioplegic solution for myocardial protection can be delivered at either cold (≈4-10⁰C) or warm (≈35-37⁰C) temperatures and there is still much debate regarding the optimal cardioplegic temperature(19).  Since the 1950s, cold crystalloid solutions were used to maintain the arrested state of the heart due to it lowering the myocardial oxygen demand and reducing the risk of ischaemic damage(20). Potassium-induced electromechanical arrest lowers the oxygen demand of the myocardium by 90%. Lower temperatures of cardioplegic solution reduce this oxygen demand by a further 5-20% which is done by reducing the myocardial basal metabolic rate(19).
Lower temperatures of cardioplegia may cause membrane rupture, denaturalisation of proteins, inhibition of Na+-K+ and Ca2+ATP systems in the sarcolemma and sarcoplasmic reticulum, and lead to oedema and calcium sequestration(21). A longer period of time is needed to rewarm the heart by reperfusion, increasing the risk of reperfusion injury and arrhythmias(19).
Hypothermia also leads to right shift of the oxyhaemoglobin dissociation curve, causing lower oxygen availability for the myocardium in cold blood cardioplegia. At 20⁰C only 50% of the total oxygen content in blood cardioplegia is available, falling to a further 30% when temperature is decreased to 10⁰C(19). Other disadvantages of cold cardioplegia include inadequate delivery of the cardioplegic solution due to sludging, cold agglutinin activation and rouleoux formation, leading to myocardial ischaemia and a delay in recovery of myocardial metabolism and function postoperatively(19).
To avoid these side-effects of cold cardioplegia, warm blood cardioplegia was brought in in the 1970s(20). Giving continuous warm cardioplegia prevents hypothermic ischaemia and also minimises reperfusion injury(19). A meta-analysis by Fan et al. found that warm cardioplegia was associated with improved postoperative cardiac index reduced cardiac markers (cTn and CK-MB) indicating less cardiocyte injury(20).
Lichtenstein et al. observed the outcomes in two groups of patients undergoing CABG post-MI. The warm group had lower 30-day mortality rate and a reduced need for postoperative IABP(19). An Emory University study however found a significantly higher rate of postoperative neurological complications in warm versus cold cardioplegia (4.5% versus 1.4%), along with more perioperative strokes with warm cardioplegia (3.1% versus 1.0% with cold). They hypothesised this was due to use of blood cardioplegia in the warm group which had higher glucose level and caused hyperglycaemia, absence of neuroprotective benefits of hypothermia, and embolic events leading to stroke(19).
With warm cardioplegia there is need for larger total volumes of cardioplegic solution, increased use of high potassium cardioplegia to eliminate episodes of electric activity, higher risk of systemic hyperkalaemia, reduced systemic vascular resistance, as well as increased use of crystalloid and alpha-agonists to maintain perfusion pressures(19).
Kuhn et al. looked at the amount of endothelial injury with each technique, quantified by measuring circulating endothelial cells (CECs), von Willebrand factor (vWF) and soluble thrombomodulin (sTM). Concentrations of all these factors were much higher with warm cardioplegia, reflecting greater endothelial injury compared to cold cardioplegia(22).  The advantages and disadvantages of each technique is summarised in Table 2.