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Eur J Cardiothorac Surg 1998;14:467-475
© 1998 Elsevier Science NL

Review article

The end of the cold era: from intermittent cold to intermittent warm blood cardioplegia

Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol BS2 8HW, UK

Received 25 May 1998; received in revised form 8 September 1998; accepted 8 September 1998.

Corresponding author. Tel.: +44 117 9283145; fax: +44 117 9299737.

	Abstract

Top Abstract Introduction Warm blood cardioplegia Intermittent warm blood... Conclusion References

 
Background: A major reduction in the energy demand of the myocardium results from the electromechanical arrest, and cooling contributes to a lesser degree to this reduction. It is from this assumption that strategies of myocardial protection, utilizing warm blood cardioplegic induction, followed by cold cardioplegia with terminal warm reperfusion before removal of the aortic cross clamp, became established as optimal myocardial protection. Continuous normothermic perfusion `closed the loop' by avoiding myocardial ischemia and linking warm induction and terminal reperfusion. A series of laboratory and clinical data confirmed the benefits of warm heart surgery on myocardial function and metabolism. The disadvantages of continuous warm blood cardioplegia including disturbance of the operative field, led surgeons to administer warm hyperkalaemic blood intermittently as a new cardioplegic strategy. Methods: This review examines the laboratory and clinical data with reference to the intermittent warm blood cardioplegia, to establish its experimental basis and place in clinical practice. Conclusions: Experimental observation and clinical application have established intermittent warm blood cardioplegia as a practical, effective and cheap myocardial protection technique, particulary with reference to coronary artery surgery.

Key Words: Myocardial protection • Cold and warm blood cardioplegia

	Introduction

Top Abstract Introduction Warm blood cardioplegia Intermittent warm blood... Conclusion References

 
Warm myocardial protection has had a striking impact on modern cardiac surgery. The renewed interest in normothermia has forced surgeons to review their everyday practice. The rationale was known for many years: the oxygen consumption of a heart, arrested by potassium-enriched normothermic blood, is 90% less than baseline values; only a slight reduction in oxygen consumption is achieved by lowering the temperature to 11°C [1]. This consideration led to the development of a continuous normothermic perfusion of the heart throughout the period of ischemia with blood [2], a technique that was adopted by many cardiac surgeons in the early 1990's. However, the inherent disadvantages of using continuous cardioplegia were the inadequate visualization of the operative field because of blood flow and the large volumes of cardioplegia. Evolution of this technique led to the introduction of intermittent warm blood cardioplegia, as a means of preserving the perceived advantages without the disadvantages. This review will outline the experimental and clinical work associated with the development of normothermic blood cardioplegia.

	Warm blood cardioplegia

Top Abstract Introduction Warm blood cardioplegia Intermittent warm blood... Conclusion References

 
The debate over the optimal temperature for cardioplegia has been one of the most important aspects of myocardial preservation. Surgeons who favour crystalloid cardioplegia agree that it should be given at low temperatures (4–10°C) to maximize myocardial cooling and metabolic inhibition [3]. However, the ideal temperature for blood cardioplegia remains controversial. Buckberg has argued that myocardial temperatures lower than 20°C are unnecessary, considering that the oxygen demand of an arrested heart at this temperature is only 0.3 ml/100 g per min [4]. Unlike asanguineous cardioplegic solutions, oxygen availability in blood cardioplegia is influenced by temperature because of the rightward shift of the oxyhaemoglobin saturation curve in response to hypothermia. In vitro studies [5] have shown that, at 20°C, only 50% of the total oxygen content of blood cardioplegia is available to the tissue and this drops an additional 30% when the temperature is lowered to 10°C. Several investigators [5] [6] have demonstrated diminished efficacy of blood cardioplegia with lower temperatures. Another criticism of intermittent hypothermic blood cardioplegia relates to the energy balance of the heart during arrest. Even a profoundly hypothermic, arrested myocardium requires some energy to maintain intracellular homeostasis. At 10°C, the arrested myocardium requires 0.14 ml of oxygen/100 g per min, approximately 95% less than normal [7]. In the absence of adequate oxygen supply, as might be present between doses of intermittent cardioplegia, the myocardium has to rely on anaerobic glycolysis for energy production. Depletion of high-energy phosphates, release of myocardial isoenzymes, and recovery of less than 100% of contractile force after intermittent hypothermic cardioplegia, suggests that anaerobic metabolism is incapable of completely meeting the metabolic demands of the cold, arrested heart [8]. Deep hypothermia may actually inhibit energy production through glycolysis to a greater degree than energy consumption [9]. In support of this, we recently demonstrated a significant reduction in the intracellular concentrations of important metabolites (glutamate, aspartate, glutamine and taurine) and high energy phosphates, during ischemia and reperfusion, in patients undergoing coronary artery surgery using cold blood St Thomas' based cardioplegic solutions [10] [11]. Other additional drawbacks to hypothermia include membrane destabilization, Na⁺-pump inhibition and resultant edema, Ca⁺⁺ sequestration and the need for a longer period of reperfusion to rewarm the heart, thereby increasing the potential for reperfusion injury and any associated reperfusion arrhythmias [12].

Two major refinements of hypothermic blood cardioplegia laid the groundwork for warm heart surgery: warm induction and terminal warm reperfusion with blood cardioplegia. The concept of warm cardioplegic induction was introduced in 1983, based on the realization that induction of cardioplegia in the ischemically damaged, energy and substrate depleted hearts is really the first phase of reperfusion [13]. Experimental and subsequent clinical data showed that warm induction could `actively resuscitate' the heart and improve its tolerance to the subsequent periods of ischemia [13]. The use of terminal warm blood cardioplegia has been demonstrated to prevent the metabolic derangement observed during reperfusion in patients undergoing coronary artery surgery using intermittent cold blood cardioplegia for myocardial preservation [14] [15]. It was logical therefore to propose that the ideal state for the heart during a cardiac operation, a state that would avoid the disadvantages of intermittent hypothermic cardioplegia, would consist of continuous normothermic perfusion with oxygenated potassium-enriched blood. The use of continuous warm blood cardioplegia would `close the loop' and allow `perfect protection' by avoiding ischemia completely [13].

Lichtenstein et al., [16] first reported the use of warm heart surgery in 1989 when they described the safe use of continuous warm cardioplegia for a patient requiring a cross-clamp time of 6.5 h. In 1991, the same group reported the results in 121 consecutive patients undergoing coronary artery surgery using continuous warm blood cardioplegia for myocardial preservation, and compared this group with an historical cohort of 133 patients who received continuous cold blood cardioplegia [17]. There was no significant difference in the overall mortality between the groups. However, patients receiving continuous warm blood cardioplegia sustained significantly fewer perioperative myocardial infarctions (MI), demonstrated a higher postoperative cardiac output and had a lower incidence of low-output syndrome. In a second retrospective study, Lichtenstein et al., observed the outcome in a selected group of patients at higher risk of perioperative complications, comparing cold and warm continuous cardioplegia [18]. Two historical cohorts of patients undergoing coronary artery bypass grafting within 6 h–1 week of an acute MI were studied. As in the first series [17], warm cardioplegia was associated with shorter reperfusion times and nearly uniform return of normal sinus rhythm. Several advantages were found in the warm group, most significantly a lower 30-day mortality rate and a decreased requirement for post-operative intra-aortic balloon pump support. There was a trend toward a reduced incidence of perioperative MI and low-output syndrome associated with the use of warm cardioplegia, although this did not reach significance. These results led Lichtenstein et al., to suggest that continuous warm cardioplegia may provide added myocardial protection for patients with limited cardiac reserve. Another trial by the Emory group confirmed similar efficacy of normothermic and hypothermic cardioplegia for myocardial preservation but raised the possibility of an increased incidence of postoperative neurological events [19]. However, systemic normothermia is not necessary to administer warm blood cardioplegia. At the Toronto Hospital, systemic temperature was allowed to drift to 33–35°C to provide neurological protection from cerebral emboli, potentially released during cannulation and aortic cross-clamping. Furthermore, the use of a partially occluding clamp technique for the construction of the proximal anastomoses and hyperglycemic crystalloid solutions employed in the Emory trial may have exacerbated intraoperative neurologic injury [20] [21].

The metabolic changes with warm blood cardioplegia
Although the clinical efficacy of warm blood cardioplegia has been convincingly demonstrated [16] [22] [23] controversies still exist regarding the effect of this strategy on myocardial metabolism.

Menasché et al. [24] investigated the effects of continuous retrograde warm blood cardioplegia on intraoperative myocardial metabolism in humans. The low oxygen extraction associated with low myocardial release of acid metabolites and lactate at the end of the ischemic time indicated that no major shift in myocardial metabolism toward anaerobic patterns occurred during aortic cross-clamping. Consequently, warm blood cardioplegia successfully prevented the energy supply-demand mismatch that defined ischemia.

Preservation of perioperative myocardial metabolism was also demonstrated by Yau et al. [25] using normothermic blood cardioplegia delivered antegradely via the aortic root at flow rates exceeding 80 ml/min with a haemoglobin concentration of 80 g/l, when compared with standard intermittent cold blood cardioplegia. Subsequently [26], the authors attempted to compare myocardial metabolic recovery after normothermic antegrade blood cardioplegia, normothermic retrograde blood cardioplegia and standard intermittent cold blood cardioplegia in patients undergoing coronary artery bypass surgery. The authors concluded that each of the three techniques of cardioplegia had distinct metabolic implications. Warm antegrade cardioplegia maximized myocardial oxygen extraction and resulted in less lactate production compared with that seen with cold blood cardioplegia, implying relative preservation of aerobic metabolism. Warm retrograde cardioplegia had the greatest myocardial lactate production, consistent with greater dependence on anaerobic metabolism. This seems to partially justify several concerns regarding the potential disadvantages of retrograde warm blood cardioplegia delivery.

Utilizing a canine model of acute global myocardial ischemia followed by a cardioplegic arrest interval, Guyton's research group [27] compared three different types of myocardial preservation technique: retrograde warm blood cardioplegia, intermittent oxygenated cold crystalloid cardioplegia and intermittent antegrade cold blood cardioplegia with terminal warm reperfusion. Analysis of the systolic performance showed no significant difference between the three groups after cross-clamp removal. Evaluation of the diastolic function utilizing a linearized stress strain regression analysis revealed that the left ventricle was stiffer in both the cold blood and the cold crystalloid groups compared with the warm blood group. The preload recruitable stroke work relationship revealed a difference between the three groups with warm blood groups significantly better after removal of the aortic cross clamp. The cold blood group was also significantly better than the cold crystalloid group. Evaluation of myocardial oxygen consumption and myocardial water content were not different among the three groups. This study suggested that warm blood cardioplegia was at least as good as cold blood cardioplegia and probably better than cold crystalloid cardioplegia in the setting of a very acute, relatively short interval of global myocardial ischemia prior to cardioplegic arrest. The differences, however, were not striking. There was no detectable difference in systolic ventricular function. The small differences in left ventricular function might be explained by a superior diastolic recovery of the warm blood hearts.

The same authors [28] then tested warm blood cardioplegia with a longer interval of myocardial ischemia utilizing a regional ischemic model which mimicked an anterior MI and more closely resembled the clinical situation of acute regional myocardial ischemia. Ventricular systolic performance recovered significantly better with warm blood cardioplegia compared with the cold cardioplegic techniques. Diastolic recovery was worse in the cold crystalloid group while no difference was observed between cold blood and warm blood groups. A significant increase in water content occurred in the cold crystalloid group but did not occur in the cold and warm blood groups, paralleling the observed changes in diastolic mechanical properties. The ATP levels from the left anterior descending coronary artery region were restored to normal levels with continuous warm blood cardioplegia. This was significantly better than intermittent cold blood cardioplegia and intermittent oxygenated cold crystalloid cardioplegia. In the non-ischemic circumflex region ATP levels were similar in the three groups. These results showed that continuous warm blood cardioplegia could resuscitate ischemic myocardium in a canine model that mimicked the clinical situation of acute coronary occlusion. Compared with the crystalloid technique, both blood techniques seemed to offer better preservation of diastolic function and prevention of myocardial edema. The warm blood technique, compared with both the cold blood and the cold crystalloid cardioplegia, led to better systolic function, better overall left ventricular function, and better restoration of high energy phosphate levels.

All this experimental data seemed to confirm the efficacy of continuous normothermic blood cardioplegia in avoiding ischemia during the aortic cross-clamp period. Other studies [29] [30], examining the myocardial metabolic effects of warm blood cardioplegia, have confirmed that myocardial ischemia is eliminated if warm blood cardioplegia is delivered in a truly uninterrupted fashion. However, in every day practice, continuous infusion of warm blood cardioplegia may obscure the operating field and therefore must be discontinued for short intervals. Indeed, it seems that an increasing number of surgeons are adopting intermittent antegrade warm blood cardioplegia, particularly because it is practical and cost-effective compared with continuous techniques.

	Intermittent warm blood cardioplegia

Top Abstract Introduction Warm blood cardioplegia Intermittent warm blood... Conclusion References

 
Experimental studies on intermittent warm blood cardioplegia are reported in Table 1.

This work represented the experimental background that led to the widespread use in clinical practice of intermittent antegrade warm blood cardioplegia (IAWBC). Calafiore and Mezzetti [32] reported the 4 years experience with IAWBC for coronary as well as aortic valve surgery procedures. The two main and distinct characteristics of this cardioplegia technique are: (a) the delivery route is exclusively antegrade and cardioplegic flow is discontinued for 85–90% of the aortic cross-clamping period; and (b) only KCl is added to blood. The maximum ischemic interval allowed during surgery was not derived on a scientific basis. Fifteen minutes of normothermic ischemia was chosen to allow construction of a difficult distal anastomosis without the need for cardioplegic reinfusion. Other authors [33] have reported clinical and metabolic results in coronary artery surgery superior to other cardioplegic methods using a semi-continuous technique, with cardioplegic delivery time of about 60% of total aortic cross-clamping time. For these authors, the interruption of cardioplegic flow, believed by some to be detrimental in retrograde cardioplegia [34] [35] is well tolerated if the antegrade route is used since it assures homogeneous distribution of cardioplegic flow and reinfusion at no longer than 15 min intervals. This allows for complete reperfusion of the heart, replenishes the energy stores and prepares the heart for another period of ischemia. Furthermore the asanguineous surgical field facilitates the operation which is performed more rapidly and with accuracy.

Mezzetti et al. [36] have recently compared the effects of intermittent antegrade warm blood cardioplegia and intermittent antegrade cold blood cardioplegia on myocardial metabolism and free radical generation during reperfusion after cardioplegic arrest in patients who underwent mitral valve replacement. Their data showed that oxidative stress is completely prevented in hearts protected by intermittent antegrade warm blood cardioplegia. The authors speculated that the absence of markers of oxidative stress at reperfusion in hearts protected with warm blood cardioplegia could be an indication that ischemia was mild and not severe enough to induce significant metabolic and structural derangements. Significant release of creatine phosphokinase (CPK) was present at reperfusion in patients receiving cold blood cardioplegia, whereas CPK arterio-coronary sinus difference did not change in patients protected with intermittent warm blood cardioplegia throughout the reperfusion period. Both groups showed significant coronary sinus lactate release at the beginning of reperfusion, but while in the warm blood group this production was rapidly converted into extraction, in the cold blood group it persisted during the reperfusion period. They suggested that this finding could be consistent with more rapid recovery of aerobic metabolism in hearts protected with warm cardioplegia, and coronary sinus lactate release, at the time of aortic declamping, might reflect the washout of metabolites accumulated during cardiopulmonary bypass rather than continued anaerobic myocardial activity.

Torracca et al. [37] have compared the protective effects of continuous warm blood cardioplegia and intermittent warm blood cardioplegia in an experimental model of a blood-perfused, isolated rabbit heart. Even though intermittent cardioplegia produced a transient but significant release of creatine kinase and lactate after each period of ischemia, it allowed a prompt and complete recovery of mechanical function and tissue content of high energy phosphates. The authors concluded that both continuous and intermittent warm blood cardioplegia exert optimal protection in the rabbit heart model and thus, intermittent warm blood cardioplegia can be safely used to improve visualization of the surgical field. In a similar study, Landymore et al. [38] analyzed the effects of intermittent antegrade cold or warm blood cardioplegia on myocardial metabolic and functional recovery during ischemia and reperfusion, in a dog heart model. Systolic function was well preserved, whereas diastolic function decreased slightly in both groups after arrest. Myocardial oxygen consumption increased during reperfusion after cold heart protection but was unchanged after warm blood. High energy phosphates decreased significantly in both groups during reperfusion. Two conclusions were reached: (a) myocardial functional recovery was well preserved, whereas metabolic recovery was impaired after either technique of myocardial preservation; (b) preserved functional recovery after multidose warm blood cardioplegia suggests that repetitive episodes of ischemia may condition the myocardium, thus preventing injury during prolonged aortic cross-clamping. This latter aspect was further investigated by the same authors [39], who wanted to determine whether warm ischemia, during the intermittent delivery of warm blood cardioplegia, would induce preconditioning during cardioplegic arrest in a dog heart model. Myocardial functional recovery was better preserved after 30 min of warm arrested ischemia in those animals preconditioned, concluding that intermittent antegrade warm blood cardioplegia may induce preconditioning during cardioplegic arrest. Although this study reports that intermittent warm blood cardioplegia may cause preconditioning, we believe that this assumption is only a means of providing a scientific rationale to the used method since repeated bouts of ischemia interspersed with short periods of reperfusion do not equate with a short ischemic interval followed by a short period of intervening reperfusion and a subsequent period of sustained ischemia (which defines ischemic preconditioning).

Using a pig heart model, Tonz et al. [40] compared the effects of continuous or intermittent warm blood cardioplegia on functional recovery, after prolonged cardiac arrest. They noticed that antegrade warm blood cardioplegia could be interrupted for up to 10 min without obvious negative effects on left ventricular function. In contrast, Kawasuji et al. [41], using near-infrared spectroscopy to monitor tissue oxygenation and myocardial oxygen metabolism during intermittent warm blood cardioplegia, noticed that episodes of ischemia longer than 10 min, resulted in less-than-optimal myocardial preservation.

A word of caution to the use of IAWBC came from Menasché [42], who has extensively studied warm blood cardioplegia in the last 10 years. For this author, the important distinction to make is not between warm and cold cardioplegia but rather between aerobic and ischemic arrest, and in this sense, `it is virtually impossible to predict, in a given patient, the time point beyond which myocardial metabolism is going to shift toward anaerobic patterns'. For this reason, the occasional discontinuation of cardioplegia administration for periods of 2 or 3 min, is likely to be inconsequential, but a cumulative interruption of 30–50% of the total cross-clamp time should more appropriately be referred to as intermittent normothermic ischemic arrest. Menasché suggested that only a combination of factors such as high haematocrit, high flow rate of delivery and continuous or almost continuous delivery, defines the technique of aerobic arrest. He coined the term `mini-cardioplegia' for this `ideal' technique of myocardial preservation, because the arresting agents (potassium/magnesium) are concentrated in a small volume of saline solution, which is continuously added to the patient's arterial blood in a cardioplegia circuitry by means of an electrically driven syringe. After the induction, cardioplegic flow is progressively decreased as long as the heart remains quiescent and is temporarily reincreased whenever there is any resumption of electromechanical activity. Menasché summarized the benefits of this type of cardioplegia in (a) improved oxygen supply because of the combination of a rightward shift of the oxyhaemoglobin dissociation curve and a greater number of available red blood cells; (b) improved control of blood volume because of the limitation of fluid overload (which greatly contributes to early postoperative extubation); (c) improved practicality because a simple electrically driven pump can substitute for more complex blood/crystalloid mixing devices; (d) improved cost-effectiveness because the expenses related to these delivery systems, various biochemical additives and, eventually, fluid-removing devices like ultrafilters or cell-saving devices are eliminated. The safety of repeated interruptions of warm blood cardioplegia was also recently evaluated by de Oliveira et al. [43] in an isolated canine heart model, with the use of phosphorus 31-magnetic resonance spectroscopy. There was full metabolic and functional recovery after three 15-min periods of ischemia during aortic cross-clamping, but a significant deterioration with 20-min periods, which was very profound when the cardioplegic flow was interrupted for up to 30 min. The authors suggested that in the clinical setting, warm blood cardioplegia could be safely interrupted for short intervals, but longer interruptions require great caution.

The debate regarding the arresting agents used with warm blood cardioplegia is mainly related to the introduction of magnesium in the cardioplegic solutions used in clinical practice. This was based on the concept that magnesium could be cardioprotective during ischemia and reperfusion because of its effect on calcium transport. Ataka et al. [44] have found that hyperkalaemic cardioplegia without magnesium does not prevent the rise in intracellular calcium during ischemia. Hyperkalaemic cardioplegic solutions partially depolarize the membrane and may open the L-type calcium-channels. Elevated intracellular calcium levels will activate a variety of cellular enzymes and transport systems as well as influencing mitochondrial function and increasing cellular energy demands [45] [46] [47]. Magnesium blocks the L-type calcium-channels, reduces calcium loading and energy demands and preserves intracellular metabolites. The effectiveness of magnesium in association with warm blood cardioplegia on myocardial function was demonstrated by Caspi et al. [48] in patients undergoing coronary artery bypass grafting. They showed that the perioperative administration of magnesium sulfate contributed to better myocardial recovery and fewer ventricular tachyarrhythmias after operation. We have recently analyzed the myocardial metabolic effects of IAWBC on patients undergoing routine myocardial revascularization, with special attention to the consequences of adding magnesium sulfate to the cardioplegic solution [49]. Patients were divided into two groups, on the basis of the use of magnesium. Levels of high energy phosphates, lactate and several amino acids were measured from left ventricular biopsies taken during ischemia and reperfusion and compared with the control values. We noticed that IAWBC with or without magnesium preserved the intracellular concentrations of ATP and amino acids during ischemia, while there was a increase in lactate levels in both groups. During reperfusion, the concentrations of ATP and amino acids decreased significantly in the group of patients in which no magnesium was added to the cardioplegia, and lactate levels remained elevated, indicating a metabolic derangement on reperfusion that was prevented by the use of magnesium in the other group of patients.

Clinical studies on IAWBC
The experimental data on IAWBC is associated with a series of clinical reports (Table 2) that have compared this cardioplegia with other commonly used methods of myocardial preservation, particularly intermittent cold blood cardioplegia (IACBC).

No difference in myocardial metabolic and functional recovery, incidence of MI, low cardiac output syndrome or death was found between IAWBC and IACBC by Landymore et al. [51] on 40 patients undergoing coronary artery surgery, indicating that a similar protection was provided with the two techniques of myocardial protection.

The report by Christakis et al. [52] focused on the right ventricular function with IAWBC or IACBC in 52 patients undergoing isolated bypass grafting. Their results showed that the right ventricular ejection fraction was greater in the warm group at 6 and 8 h postoperatively and the right ventricular end-diastolic volume was less in the warm group 8 h postoperatively. No differences in pulmonary arterial pressures or right ventricular stroke work index was found between the groups. They concluded that despite intermittent normothermic ischemia occurring at half the cross-clamp time, patients receiving warm cardioplegia maintained right ventricular haemodynamics after bypass grafting.

To evaluate the effectiveness of IAWBC in aortic valve replacement, Calafiore et al. [53] compared the clinical results of two groups of patients receiving either IAWBC or IACBC. Mortality was similar in both groups, but no patients in the warm group died of cardiac-related causes. More patients in the warm group recovered spontaneous rhythm, with shorter extubation time and less bleeding compared with the cold group, and as a consequence, shorter intensive care unit stay and postoperative hospital stay. Furthermore, IAWBC was associated with a reduced incidence of low output syndrome, ventricular arrhythmias and the need for lidocaine infusion, and in conclusion, with lower cardiac-related mortality and morbidity.

Interrupting cardioplegic flow, during construction of distal anastomoses, has been shown experimentally by some authors to be deleterious [54] [55]. Lichtenstein et al. [56] studied the relation between the intermittent administration of warm blood cardioplegia and the frequency of adverse perioperative events. IAWBC was used in 720 patients undergoing coronary bypass surgery. Intermittency was calculated according to the longest single ischemic time in min per patient (longest time off cardioplegia, LTOC) and also as a proportion of the cross-clamp time per patient (percentage of time off cardioplegia, PTCO). PTCO and LTCO were divided into quartiles and related to prespecified composite outcomes of mortality, enzymatic MI and low output syndrome. The data showed that periods of normothermic myocardial ischemia in the presence of electromechanical arrest were well tolerated and potentially protective provided that any single ischemic interval was <13 min.

Calafiore et al. [57] reviewed their clinical experience in 500 elective or urgent patients undergoing coronary artery bypass grafting using either IAWBC or IACBC. The most striking difference between the two groups was morbidity. Five patients in the cold group needed circulatory assistance at the time of weaning from cardiopulmonary bypass; 20 patients in this group experienced low output syndrome, intra-aortic balloon counterpulsation being required in four of them. No patients in the warm group needed circulatory assistance and only one patient had low output syndrome. No patients in this group required intra-aortic balloon counterpulsation. The incidence of postoperative MI was lower in the warm group but the difference was not statistically significant. There was a lower mortality and no cardiac related deaths in the warm group compared with the cold group, in which six patients died of MI.

	Conclusion

Top Abstract Introduction Warm blood cardioplegia Intermittent warm blood... Conclusion References

 
This review has attempted to trace the experimental and clinical studies underlying the evolution of intermittent warm blood cardioplegia. Presently, this technique appears to be yet another alternative to the many myocardial protection strategies available. Experimental, metabolic and clinical evidence indicate that intermittent warm blood cardioplegia is safe and effective. Nevertheless, concerns still exist regarding the interruption of cardioplegic flow as a possible way of producing periods of normothermic ischemia, and the safe duration of these ischemic intervals. This is particularly true in high risk patients in whom intentionally inflicting an ischemic injury to an already severely compromised heart may not be as safe as occasionally thought. Future studies must focus on establishing conditions to detect and prevent myocardial ischemia during the period of aortic clamping, creating the optimal conditions for normothermic blood cardioplegia. In the mean time perhaps the era of cold cardioplegia is not quite finished but its days are numbered.

	References

Top Abstract Introduction Warm blood cardioplegia Intermittent warm blood... Conclusion References

 

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