Terminal Warm Blood Research Articles

Effects of Del Nido and Terminal Warm Blood Cardioplegia on Myocardial Protection and Rhythm in Isolated CABG Patients.

To investigate the effect of using del Nido cardioplegia+terminal hot-shot blood cardioplegia on myocardial protection and rhythm in isolated coronary bypass patients. A total of 122 patients were given cold (+4-8C') del Nido cardioplegia antegrade and evaluated. Del Nido+terminal warm blood cardioplegia (TWBCP) was applied to 63 patients out of 122 patients, while del Nido cardioplegia alone was applied to the other 59 patients. The preoperative and postoperative data of the patients were recorded and compared. There was a significant statistical difference between the groups, in terms of volume with more cardioplegia in the del Nido+terminal warm blood cardioplegia group. Although there was no significant difference between cardiac arrest times in both groups, a statistically significant difference was found in the del Nido+terminal warm blood cardioplegia group in the starting to work time of the heart. No difference found between the groups regarding myocardial preservation. We can add a return to spontaneous sinus rhythm to the advantages of terminal warm blood cardioplegia and del Nido cardioplegia in literature. We think it would be a good strategy to extend the safe ischemic time limit of del Nido to 120 minutes with a terminal warm blood cardioplegia. It seems that cardioplegia techniques that will be developed by adding the successful and superior results of crystalloid cardioplegia applications, such as single dose del Nido in various open heart surgery operations and the superior myocardial return effects of terminal warm blood cardioplegia, will be used routinely in the future.

Effect of Cardioplegia for Myocardial Protection in Pediatric Cardiac Surgery: A Network Meta-Analysis

Cardioplegia has been widely used to reduce myocardial injury during pediatric cardiac surgery; however, which cardioplegia solution has the best protective effect has not been established. Thus, we compared the myocardial protective effects of different cardioplegia solutions used in pediatric cardiac surgery. Seven databases were searched to identify the relevant randomized controlled trials. A network meta-analysis with a Bayesian framework was conducted. The outcomes included the following biochemical and clinical outcomes: serum concentrations of the creatine kinase-myocardial band at 6 h postoperatively; cardiac troponin I (cTnI) at 4, 12, and 24 h postoperatively; spontaneous beating after declamping; postoperative arrhythmias; inotropic support percentage and duration; mechanical ventilation hours; intensive care unit stay in days; hospital stay in days; and mortality. The group treated with cold crystalloid cardioplegia (cCCP) was chosen as the control group. The 22 studies involved 1529 patients. Six types of cardioplegia solutions were described in these studies, including cold blood cardioplegia, cCCP, del Nido, histidine-tryptophan-ketoglutarate (HTK), terminal warm blood cardioplegia, and warm blood cardioplegia (wBCP). The serum concentrations of the 24-h cTnI with wBCP (MD = −2.52, 95% CI: −4.74 to −0.27) was significantly lower than cCCP. The serum concentrations of the 24-h cTnI with HTK (MD = 4.91, 95%CI: 2.84–7.24) was significantly higher than cCCP. There was no significant difference in other biochemical and clinical outcomes when compared to cCCP. In conclusion, wBCP may have a superior myocardial protective effect with lower 24-h cTnI levels postoperatively and similar clinical outcomes after pediatric cardiac surgery.

Superior restoration of left ventricular performance after prolonged single-dose del Nido cardioplegia in conjunction with terminal warm blood cardioplegic reperfusion

ObjectivesAn incomplete restoration of left ventricular contractility after del Nido cardioplegia was noted in our recent study. This study tested the hypothesis that terminal warm blood cardioplegia promotes a prompt restoration of left ventricular performance after a prolonged single-dose del Nido cardioplegia. MethodsFourteen piglets were subjected to 120 minutes of arrest by del Nido cardioplegia without terminal warm blood cardioplegia (del Nido cardioplegia group; n = 7) or with terminal warm blood cardioplegia before reperfusion (terminal warm blood cardioplegia group; n = 7). The other 7 piglets underwent total cardiopulmonary bypass without ischemia/reperfusion for 150 minutes (control group). Left ventricular function was assessed by percent recovery of end-systolic elastance as the contractility and percent end-diastolic pressure–volume relationship as the compliance using a conductance catheter. Troponin T and the mitochondrial score were also measured. ResultsDepressed percent recovery of end-systolic elastance was sustained in the del Nido cardioplegia group, and a prompt restoration of end-systolic elastance was achieved using terminal warm blood cardioplegia (57.9 ± 17.8 vs 94.7 ± 13.1, P < .028). Percent end-diastolic pressure–volume relationship at the early phase was better in the terminal warm blood cardioplegia compared with the del Nido group (88.5 ± 24.0 vs 101.4 ± 16.8, P = .050). Troponin T was higher in the terminal warm blood cardioplegia compared with the control group (0.80% ± 0.21% and 1.49% ± 0.31%, respectively, P = .002). The mitochondrial score was equivalent in all groups. Spontaneous restoration to sinus rhythm was more frequent in the terminal warm blood cardioplegia group than in the del Nido cardioplegia group (6/7 vs 1/7, P < .028). ConclusionsThe supplementary use of terminal warm blood cardioplegia achieved prolongation of the safe ischemic time up to 120 minutes for a single-dose application.

COMPARISON STUDY: INTERMITTENT ANTIGRADE WARM CARDIOPLEGIA VERSUS ANTIGRADE COLD INTERMITTENT BLOOD CARDIOPLEGIA FOR MYOCARDIAL PROTECTION DURING ELECTIVE ON PUMP CORONARY ARTERY BYPASS GRAFTING IN EARLY POST-OPERATIVE PERIOD

Background: Defending the heart against potential damage during cross-clamping is the most important and vital step to ensuring a successful surgical outcome(1). The creation of cardioplegia solutions was one of the major advances in cardiac surgery that allowed surgeons to conduct complicated surgical procedures to avoid myocardial injury (14). Treating cardioplegia at a cool temperature would be a significant factor in lowering myocardial metabolism. However, the reduction in myocardial metabolism due to hypothermia, compared with that achieved by diastolic arrest, is usually very negligible. Since Normothermias enzymatic and cellular processes work better (7). Owing to the propensity of the heart to resume electrical operation during normothermia, however, this must be administered consistently or only with short interruptions (4). Terminal warm blood cardioplegia (hot shot) is normally done just before the elimination of the aortic cross-clamp since it has been demonstrated that myocardial metabolism is increasing (23). Methods: A prospective controlled randomised study (200 hundred patients aged 40 to 65 years of both sexes underwent elective CABG pump surgery) will be included. They will be divided into three groups of patients: Group I:includes 100 Patients who received intermittent cold blood cardioplegia. Group II:includes 100 Patients who received intermittent warm blood cardioplegia with controlled reperfusion for 3 minutes before aortic unclamping. Study made from January, 2019 to August, 2020, at National Heart Institute.All patients were thoroughly evaluated preoperatively, intraoperatively, and postoperatively. Results: We hypothesized that in our patient cohort, warm blood cardioplegia could be as successful as or even better than the conventional antegrade cold blood cardioplegia. Patients were randomised into two similar blocks, each of which consisted of 100 patients, each of whom obtained one of the two cardioplegic solutions. Our analysis did not indicate a statistically important difference in the post-operative release of myocardial biomarkers (Troponin I) &amp; CK in both classes. This finding did not significantly reflect the clinical outcome of our patient, which may indicate similar myocardial protection in primary low-risk CABG patients for both cold and warm blood cardioplegia. Conclusion: During the time of cardiac arrest, both methods tend to enable an equal and adequate approach for myocardial defence. To attain improved myocardial defence, warm blood cardioplegia needs a shorter administration interval. Therefore, the choice between one type of cardioplegia and the other remains at the discretion of the surgeon. The statistically minor variation found in the release of myocardial enzymes did not translate into distinct clinical results.

Role of terminal warm blood cardioplegia in complex congenital heart surgery.

Introduction Myocardial protection is vital to ensure successful open heart surgery. Cardioplegic solution is one method to achieve good myocardial protection. Inevitably, ischemia-reperfusion injury occurs with aortic crossclamping. Histidine-tryptophan-ketoglutarate solution is a frequently used cardioplegia for complex congenital heart surgery. We postulated that addition of terminal warm blood cardioplegia before removal of the aortic crossclamp might improve myocardial protection. Method A randomized controlled trial was conducted on 109 cyanotic patients aged, 1 to 5 years who underwent complex biventricular repair. They were divided into a control group of 55 patients who had histidine-tryptophan-ketoglutarate only and a treatment group of 54 who had histidine-tryptophan-ketoglutarate with terminal warm blood cardioplegia. Endpoints were clinical parameters, troponin I levels, and caspase-3 as an apoptosis marker. Results The incidence of low cardiac output syndrome was 34%, with no significant difference between groups (35.2% vs. 33.3%, p = 0.84). The incidence of arrhythmias in our treatment group was lower compared to the control group (36% vs. 12%, p = 0.005). Troponin I and caspase-3 results did not show any significant differences between groups. For cases with Aristotle score ≥ 10, weak expression of caspase-3 in the treatment group post-cardiopulmonary bypass was lower compared to the control group. Conclusion For complex congenital cardiac surgery, the addition of terminal warm blood cardioplegia does not significantly improve postoperative clinical or metabolic markers.

Synergistic effects of remote perconditioning with terminal blood cardioplegia in an in vivo piglet model.

This study tested the hypothesis that remote perconditioning offers effective and synergistic cardioprotection to terminal warm blood cardioplegia for prompt ventricular recovery after prolonged cardioplegic arrest in an in vivo piglet model. Twenty-four piglets were subjected to 120 min of single-dose cardioplegic arrest and were divided into 4 groups according to the mode of reperfusion: control (simple aortic unclamp), remote perconditioning, terminal warm blood cardioplegia or remote perconditioning + terminal warm blood cardioplegia; remote perconditioning (4 cycles of 5-min ischaemia-reperfusion of the lower limb) was applied prior to aortic unclamping. Left ventricular systolic and diastolic functions were assessed by pressure-volume loop analysis at baseline and after 60 min of reperfusion. Biochemical injury was evaluated by plasma troponin T level. The control group showed decreased end-systolic elastance, preload recruitable stroke work and inverse of end-diastolic pressure-volume relationship of 51.3 ± 14.0%, 46.1 ± 22.5% and 34.8 ± 14.9%, respectively. Percentage recovery of end-systolic elastance and preload recruitable stroke work were significantly better with terminal warm blood cardioplegia (with or without remote perconditioning) (end-systolic elastance: 95% confidence interval, 38.6-84.1; preload recruitable stroke work: 95% confidence interval, 0.4-54.3). Percentage recovery of inverse of end-diastolic pressure-volume relationship was significantly better in the remote perconditioning groups (with or without terminal warm blood cardioplegia) (95% confidence interval, 1.6-41.6). No synergistic effects of remote perconditioning and terminal warm blood cardioplegia on troponin T release were noted. Remote perconditioning offers promising synergistic cardioprotection to terminal warm blood cardioplegia, implicating potential clinical benefit by contributing to prompt left ventricular functional recovery during paediatric open-heart surgery.

Reply to Kurkluoglu et al.

We thank Dr Kurkluoglu et al. for their extremely interesting letter that raises several fascinating points [1]. I fully agree with the anatomical pathway of the myocardium’s venous drainage [2]. However, I should mention the differences in the routes of effluent between antegrade and retrograde administration. The retrograde administration of the solution through the coronary sinus of the human heart has two general pathways of flow. The first is the greater venous system through the capillaries, coronary arteries and then exiting into the aortic root. In the human heart, approximately one quarter of retrograde cardioplegia follows this pathway. The other major avenue for the retrograde administration of the solution is through the venous channels that communicate with the ventricular chambers. In the clinical setting, it is noted commonly that a substantial fraction of retrograde solution is shunted into the ventricular chambers. In this experimental explanted human heart model, nearly 80% of the solution administered through the coronary sinus was recovered in the ventricular chambers [3]. Therefore, not much time was required for adequate volume loading to the left ventricle. The average time interval between terminal warm blood and heart beating was 8.1 ± 2.8 min. During this time interval, ring annuloplasty was usually performed to save time. In our series, no low-output syndrome and myocardial infarction occurred. However, the suggestion by Dr Kurkluoglu is rich in implication. It is important to obtain the developed left ventricular pressure information directly via the aortic root pressure monitoring port of the root vent needle [4]. Extremely high pressure may predispose to myocardial injury. In this case, the mean left ventricular pressure was 84.6 mmHg. All patients were readily weaned from cardiopulmonary bypass with a low-dose inotropic agent. According to our clinical data, no endocardial injury was suspected. Furthermore, we have been undertaking research on the mitochondrial ultrastructure of ventricular biopsy specimens. We will present the result in the near future. Then again, we would like to thank Dr Kurkluoglu et al. for their constructive comments and appreciate their interest in our report. We hope to augment further understanding and promote the widespread implementation of the retrograde cardioprotective beating test.

Reversal of oxidant-mediated biochemical injury and prompt functional recovery after prolonged single-dose crystalloid cardioplegic arrest in the infantile piglet heart by terminal warm-blood cardioplegia supplemented with phosphodiesterase III inhibitor

The benefit of terminal blood cardioplegia (TWBCP) is insufficient after prolonged ischemia associated with inevitable oxidant-mediated injury by this modality alone. We tested the effects of TWBCP supplemented with high-dose olprinone, which is a phosphodiesterase III inhibitor, a clinically available compound with the potential to reduce oxidant stress and calcium overload. We evaluated the effects with respect to avoiding oxidant-mediated myocardial reperfusion injury and prompt functional recovery after prolonged single-dose crystalloid cardioplegic arrest in a infantile piglet cardiopulmonary bypass (CPB) model. Fifteen piglets were subjected to 90 min of cardioplegic arrest on CPB, followed by 30 min of reperfusion. In group I, uncontrolled reperfusion was applied without receiving TWBCP; in group II, TWBCP was given; in group III, TWBCP was supplemented with olprinone (3 μg/ml). Myocardial performance was evaluated before and after CPB by a left ventricular (LV) function curve and pressure-volume loop analyses. Biochemical injury was determined by measurements of troponin-T and lipid peroxide (LPO) in coronary sinus blood. Group III showed significant LV performance recovery (group I, 26.5% ± 5.1%; group II, 42.9% ± 10.8%; group III, 81.9% ± 24.5%, P < 0.01 vs. groups I and II), associated with significant reduction of troponin-T and LPO at the reperfusion phase. No piglets in group III needed electrical cardioversion. We concluded that TWBCP with olprinone reduces myocardial reperfusion injury by reducing oxidant-mediated lipid peroxidation, and it accelerates prompt and persistent LV functional recovery with suppression of reperfusion arrhythmia.

Single Dose Inamrinone in Terminal Warm Cardioplegia in On-Pump Coronary Artery Bypass Patients

Background: Phosphodiesterase inhibitors (PDI) are used in cardiac surgery to improve and stabilize cardiac function after surgery. The aim of this study is to evaluate changes in hemodynamics and early outcomes when PDI (Inocor/inamrinone) is given in terminal warm blood cardioplegia to on-pump CABG only patients and compare results with patients who did not receive the drug. Material and methods: From April 2003 through September 2004 241 pts underwent elective on-pump CABG only surgery. 141 pts received Inocor in the terminal warm blood cardioplegia (Group 1) and 100 pts did not (Group 2). Results: Demographic data, preoperative EuroSCORE risk scores and operative details were similar. Of pts preoperatively in sinus rhythm (SR) 80.15% in Group 1 and 69.79% in Group 2 regained spontaneous SR (p = 0.07) after release of crossclamp. Inotropic support was needed in 5 pts in Group 1 and in 12 pts in Group 2, p = 0.02. Post cardiopulmonary by-pass (CPB) IABP support was needed for 4 pts in Group 2 and none for Group 1 pts, p = 0.01. There was no operative mortality in either Group and hospital/30 day mortality was similar (3/2.13% vs 3/3.00%, p = 0.69). There were no statistical difference in stay in postoperative intensive care unit (p = 0.15), total hospital stay (p = 0.07), appearance of postoperative atrial fibrillation (p = 0.23) or appearance of postoperative kidney injury (p = 0.27). Post CPB cardiac index improved 16.90% in Group1but decreased 1.49% in Group 2, p < 0.0001. Mean arterial pressure decreased 7.46%in Group 1 pts and 5.08% in Group 2 pts, p = 0.002, but no pts in either Group needed medication for too low blood pressure. Systemic vascular resistance decreased 28.40% in Group 1 and 9.02% in Group 2, p < 0.0001. Conclusions: Inamrinone in terminal warm blood cardioplegia (hot shot) is safe and effective way to improve and stabilize cardiac function after on-pump CABG surgery but does not affect short-term outcomes.

A comparison of different management techniques for myocardial protection in acyanotic congenital cardiac patients

Aim: It has already been shown that terminal warm blood cardioplegia (TWBC) supports myocardial protection in pediatric patients when it is administered after cold blood cardioplegia. However, the myocardial protective effects of TWBC applied after cold crystalloid cardioplegia (CCC) is still a subject of debate. Materials and methods: Twenty acyanotic congenital cardiac patients were randomly divided into 2 groups of 10. In the control group (CG), moderate hypothermia, topical cooling, and cold crystalloid cardioplegia were performed for the protection of the myocardium. In the other group (TWBCG), the same procedure was supported using TWBC just before the unclamping of the aorta. Blood samples were analyzed to discover the progression of anaerobic energy metabolism potentially causing injury of the myocardium during the ischemic, reperfusion, and postoperative period. Results: There were no significant statistical differences in age, body weight, mean pulmonary artery pressure, operation procedure, cardiopulmonary bypass and aortic cross clamping time, period of respiratory support, and intensive care unit and hospital stay. Also measurement of serum cardiac troponin T (TnT), creatine kinase MB(CK-MB), and lactate levels preoperatively, just after the release of the cross clamp and at the time of postoperative 4, 12, 24, and 48 h showed no significant differences either. Conclusion: TWBC was not able to enhance the myocardial protective effects in acyanotic congenital cardiac patients when performed in addition to CCC.

Long-Term Outcome of Lung and Heart-Lung Transplantation for Idiopathic Pulmonary Arterial Hypertension

The survival after lung and heart-lung transplantation for idiopathic pulmonary arterial hypertension has been reportedly the lowest among the major diagnostic categories of lung transplant recipients. Retrospective analysis was performed for lung and heart-lung transplant recipients for idiopathic pulmonary arterial hypertension from 1982 to 2006. The patients were divided into 2 groups, based on the era; group 1: 1982 to 1993, and group 2: 1994 to 2006. Since 1994, we have introduced our current protocols including prostaglandin E1 and nitroglycerin for donor lung preservation, and lung protection with cold and terminal warm blood pneumoplegia as well as immunosuppression with alemtuzumab induction. These modifications were introduced in different years over a wide span of time (1994 to 2003). Group 1 had 59 patients (35 +/- 1 years old, ranging 15 to 53, 20 male and 39 female) with 7 single lung, 11 double lung, and 41 heart-lung, whereas group 2 had 30 (43 +/- 2 years old, ranging 17 to 65, 9 male and 21 female) with 2 single, 20 double, and 8 heart-lung transplantations. The recipient age was significantly (p = 0.004) higher in group 2, and group 2 had significantly older (35 +/- 3 vs 26 +/- 1, p = 0.002) and more female donors (73% vs 41%, p = 0.007) compared with group 1. The actuarial survival was significantly (p = 0.004) better in group 2 with 86% at 1 year, 75% at 5 years, and 66% at 10 years compared with group 1 with 58% at 1 year, 39% at 5 years, and 27% at 10 years. With our current pulmonary protection and immunosuppression, the long-term outcome of lung and heart-lung transplantation for idiopathic pulmonary arterial hypertension is excellent.

Retrograde Hot-Shot Cardioplegia in Patients With Left Ventricular Hypertrophy Undergoing Aortic Valve Replacement

Intermittent antegrade cold-blood cardioplegia followed by terminal warm-blood cardioplegic reperfusion or hot-shot is reported to reduce myocardial injury in the setting of coronary surgery. The efficacy of this cardioplegic technique in patients with left ventricular hypertrophy secondary to aortic stenosis remains uncertain. Thirty-six patients with left ventricular hypertrophy undergoing aortic valve replacement were prospectively randomized to cold-blood cardioplegia either alone (cold-blood cardioplegia group) or with retrograde hot-shot (hot-shot group). Reperfusion injury was assessed by measuring myocardial levels of adenosine triphosphate and lactate in left and right ventricular biopsies taken 5 minutes after institution of cardiopulmonary bypass and 20 minutes after removal of cross-clamp using high-performance liquid chromatography and enzymatic techniques. Myocardial injury was assessed by serial release of troponin I up to 48 hours postoperatively. Overall clinical outcome was prospectively collected. Baseline and intraoperative characteristics were similar between groups. In the hot-shot group, there were no significant changes in the myocardial concentration of adenosine triphosphate and lactate in both left and right ventricular biopsies after reperfusion. In the cold-blood cardioplegia group, there was a trend to a fall in adenosine triphosphate levels in the left and right ventricular biopsies after reperfusion, but this reached statistical significance only in the right ventricle. Troponin I release was raised in both groups at 4 and 12 hours after surgery (p < 0.05), but did not reach levels of myocardial infarction. The terminal retrograde hot-shot reperfusion does not add any extra benefit to antegrade cold-blood cardioplegia in preventing myocardial injury in patients with left ventricular hypertrophy undergoing aortic valve replacement. Nevertheless, it appears to reduce ischemic stress in the right ventricle. There was no difference in clinical outcome between groups.

Terminal Warm Blood Cardioplegia in Mitral Valve Replacement: Prospective Study

Terminal warm blood cardioplegia has had a profound impact on cardiac surgery, especially in coronary artery bypass surgery, but there have been few studies on its use in mitral valve replacement. The purpose of this study was to determine whether terminal warm blood cardioplegia offers any advantages in mitral valve replacement. Forty patients with mitral valve disease were prospectively randomized to one of two groups of 20 with different techniques of myocardial protection: group A had cold blood cardioplegia, and group B had cold blood cardioplegia with terminal warm blood cardioplegia. Intraoperative and postoperative variables were used to assess primary outcomes. Postoperative troponin T release was measured as a secondary outcome. Improved spontaneous recovery of sinus rhythm was observed in group B, but the difference was not significant. The maximum doses of inotropics, duration of inotropic support, intensive care unit stay, and postoperative left ventricular ejection fraction were similar in both groups. Troponin T release at 0 and 6 h postoperatively was not different between the two groups. This study did not find any benefit of terminal warm blood cardioplegia in either clinical outcome or troponin T release after mitral valve replacement.

A Comparison of 250 and 500 mL of Terminal Warm Blood Cardioplegia After Global Myocardial Ischemia:. A Prospective Randomized Study

Controlled reperfusion with terminal warm blood cardioplegia (TWBC) improves myocardial performance after global ischemia. However, the optimum volume required is unknown. Fifty patients undergoing elective coronary artery bypass graft surgery were prospectively randomized to receive either 250 or 500 mL of TWBC. During TWBC delivery, and for 10 minutes after cross-clamp removal, samples were taken from the aorta and coronary sinus to measure the hydrogen ion, lactate, and oxygen content. At the end of TWBC delivery, the 500 mL group had significantly less hydrogen ion washout (p = 0.006) compared with the 250 mL group. Also, more hydrogen ions (p = 0.02) and lactate (p = 0.02) had been washed out during the entire period of TWBC delivery in the 500 mL group compared with the 250 mL, indicating better metabolic recovery. By 4 minutes after aortic cross-clamp removal, hydrogen ion and lactate washout, as well as oxygen extraction was similar in the two groups. However, the time to return to regular mechanical activity was prolonged in the 500 mL group, 5.8 (3) versus 4.6 (3) minutes in the 250 mL group (p = 0.05). Though there was no difference in postoperative Troponin T levels, eight patients in the 500 mL group versus four in the 250 mL group required ionotropic support (p = 0.1). A total of 500 mL of hotshot achieves a better metabolic state after hotshot delivery. However, there is no clinical benefit or improvement in the postoperative Troponin T release suggesting that in a short ischemic time, 500 mL TWCB has a limited clinical benefit.

Myocardial metabolic changes during pediatric cardiac surgery: A randomized study of 3 cardioplegic techniques

BackgroundBlood cardioplegia and terminal warm blood cardioplegic reperfusion (“hot shot”) reduce myocardial injury and improve metabolic recovery in hypoxic but not normoxic experimental models. However, there is little evidence of a benefit of either technique in pediatric clinical practice compared with crystalloid cardioplegia. MethodsPediatric patients undergoing cardiac surgery were randomized to receive intermittent antegrade cold crystalloid cardioplegia, cold blood cardioplegia, or cold blood cardioplegia with a hot shot. Right ventricular biopsy specimens were collected before ischemia, at the end of ischemia, and 20 minutes after reperfusion. Cellular metabolites were analyzed. In acyanotic patients postoperative serum troponin I levels were also measured at 1, 4, 12, 24, and 48 hours. ResultsOf 103 patients recruited, 32 (22 acyanotic and 10 cyanotic), 36 (24 acyanotic and 12 cyanotic), and 35 (25 acyanotic and 10 cyanotic), respectively, were allocated to the groups receiving cold crystalloid cardioplegia, cold blood cardioplegia, and cold blood cardioplegia with a hot shot. Cyanotic patients were younger, with longer crossclamp times. There were no significant differences in clinical outcomes between cardioplegic methods. The cardioplegic method had no overall effect in terms of adenosine triphosphate, ln(adenosine triphosphate/adenosine diphosphate), or ln(glutamate) in acyanotic patients (P = .11, P = .66, and P = .30, respectively). Also, there was no significant difference between groups in troponin I release. However, in cyanotic patients cold blood cardioplegia with a hot shot significantly reduced the decrease in adenosine triphosphate, ln(adenosine triphosphate/adenosine diphosphate), and glutamate observed at the end of ischemia and after reperfusion compared with the decrease seen in those receiving cold crystalloid cardioplegia (P = .002, P = .003, and P = .008, respectively), with cold blood cardioplegia representing an intermediate. ConclusionsFor cyanotic patients (younger, with longer crossclamp times), cold blood cardioplegia with a hot shot is the best method of myocardial protection. For acyanotic patients (older, with shorter crossclamp times), cardioplegic technique is not critical.

Cardioprotective effects and the mechanisms of terminal warm blood cardioplegia in pediatric cardiac surgery

Objectives Terminal warm blood cardioplegia has been shown to enhance myocardial protection in adult patients. However, the cardioprotective effects and the mechanisms of terminal warm blood cardioplegia in pediatric heart surgery were still unknown. Methods One hundred three consecutive patients were prospectively randomized to one of two groups. In the control group (n = 52), myocardial protection was achieved with intermittent hyperkalemic cold blood cardioplegia and topical cardiac cooling. In the terminal warm blood cardioplegia group (n = 51), this was supplemented with terminal warm blood cardioplegia before the aorta was declamped. Arterial and coronary sinus blood samples were analyzed to determine myocardial energy metabolism and tissue injury. Results There were no significant differences between the two groups in age (5.5 ± 0.6 years in the control group vs 5.6 ± 0.5 years in the terminal warm blood cardioplegia group), body weight (17.2 ± 1.4 kg in the control group vs 19.8 ± 1.7 kg in the terminal warm blood cardioplegia group), percentage of cyanotic heart diseases (50% in the control group vs 51% in the terminal warm blood cardioplegia group), number of patients who required right ventriculotomy (33% in the control group vs 39% in the terminal warm blood cardioplegia group), cardiopulmonary bypass time (194 ± 12.1 minutes in the control group vs 177 ± 8.6 minutes in the terminal warm blood cardioplegia group), aortic crossclamp time (83.3 ± 5.9 minutes in the control group vs 82.3 ± 5 minutes in the terminal warm blood cardioplegia group), lowest rectal temperature (27.4 ± 0.3°C in the control group vs 28.1 ± 0.3°C in the terminal warm blood cardioplegia group), and myocardial temperature (9.6 ± 0.6°C in the control group vs 9.6 ± 0.7°C in the terminal warm blood cardioplegia group). Spontaneous defibrillation occurred after reperfusion in 80% in the terminal warm blood cardioplegia group, which was significantly ( P < .05) higher than the control group (62%). The lactate extraction rate at 60 minutes of reperfusion was significantly ( P < .05) higher in the terminal warm blood cardioplegia group (9.0 ± 2.8%) than the control group (−3.3 ± 2.4%). The postreperfusion values of cardiac troponin T (7.4 ± 0.6 ng/mL vs 11.2 ± 1.0 ng/mL at 6 hours; 4.6 ± 0.6 ng/mL vs 9.3 ± 1.6 ng/mL at 18 hours) and heart-type fatty acid binding protein (137 ± 28 ng/mL vs 240 ± 30 ng/mL at 2 hours; 88 ± 19 ng/mL vs 162 ± 26 ng/mL at 3 hours) were significantly ( P < .05 vs the control group) lower in the terminal warm blood cardioplegia group. Conclusion Terminal warm blood cardioplegia enhances myocardial protection in pediatric cardiac surgery by an improvement in aerobic energy metabolism and a reduction of myocardial injury or necrosis.

Terminal Warm Blood Cardioplegia Improves Cardiac Function Through Microtubule Repolymerization

Background. To elucidate the mechanisms responsible for the beneficial effects of terminal warm blood cardioplegia, we studied dynamic change in microtubules induced by cold cardioplegia followed by rewarming. Further, we investigated the relationship between cardiac function and morphologic changes in microtubules caused by hyperkalemic, hypocalcemic warm cardioplegia during initial reperfusion. Methods. In protocol 1 isolated rat hearts were perfused at 37°C with Krebs-Henseleit buffer (KHB). After 3 hours of hypothermic cardiac arrest at 10°C, hearts were reperfused at 37°C with one of two buffers: group C, 60-minute reperfusion with KHB (K +, 5.9 mmol/L; Ca 2+, 2.5 mmol/L); and group TC, 10-minute initial reperfusion with modified KHB (K +, 15 mmol/L; Ca 2+, 0.25 mmol/L), followed by 50 minutes of reperfusion with KHB. Cardiac function after reperfusion was determined as a percentage of the prearrest value. In protocol 2 hearts were perfused at 37°C with KHB containing colchicine (10 −5 mol/L) for 60 minutes. Results. There was spontaneous contractile recovery after 10 minutes of initial reperfusion in hearts from group TC as well as improved cardiac function after 15, 30, and 60 minutes of reperfusion compared with that in group C. Immunohistochemical staining and immunoblot analysis demonstrated microtubule depolymerization during hypothermic cardiac arrest and complete repolymerization after 10 minutes of reperfusion with warm buffers in both groups. Colchicine-induced microtubule depolymerization is associated with deterioration of cardiac function. Conclusions. One mechanism responsible for improved cardiac function mediated by terminal warm blood cardioplegia is the restart of contraction after complete microtubule repolymerization.

Early recovery after valvular heart surgery

There have been published not a few reports concerning the early recovery from heart surgery. But most of them were restricted in CABG cases. We report our efforts and its results about the early recovery from valvular heart surgery. To make a contribution to the early recovery we have made some efforts since 1995, including normothermic perfusion, low-dose fentanyl and introduction of terminal warm blood cardioplegia. As the results, the tracheal intubation period was shortened from 12.6 +/- 5.3 (hour) to 6.7 +/- 4.1. The number of the cases who had tracheal extubation in the operative day increased from 27% to 84%. The postoperative cardiac function was satisfactory and there were no abdominal or neurologic disturbances among the patients those who were entered into the early recovery protocol. We obtained satisfied early recovery in safe after valvular heart surgery.

Myocardial Oxygenation During Terminal Warm Blood Cardioplegia

Background. Terminal warm blood cardioplegia accelerates myocardial metabolic recovery. The process of myocardial oxygenation during terminal warm blood cardioplegia and its optimal administration are not clear. Methods. We measured the myocardial tissue oxygen saturation (SO 2) during reperfusion using near-infrared spectroscopy. Twenty-four dogs underwent 1 hour of ischemic arrest with cold crystalloid cardioplegia. They were then divided into four equal groups. Group 1 dogs received normal blood reperfusion. The other dogs received 15 mL/kg of terminal warm blood cardioplegia at 80 mm Hg in group 2 or at 60 mm Hg in group 3, and 30 mL/kg of cardioplegia at 60 mm Hg in group 4, followed by blood reperfusion. Results. In group 1, the SO 2 increased gradually during the early reperfusion and decreased transiently during the late reperfusion. In group 2, the SO 2 increased rapidly but it decreased transiently during blood reperfusion. In groups 3 and 4, the SO 2 increased rapidly and remained at high levels during the blood reperfusion. Reperfusion ventricular fibrillation occurred along with a SO 2 decrease only in groups 1 and 2. The postischemic troponin-T levels of groups 3 and 4 were lower than that of group 1. The functional recovery in group 4 was better than those in the other three groups. Conclusions. Terminal warm blood cardioplegia accelerates the early SO 2 increase and abolishes the SO 2 decrease during subsequent reperfusion and reduces the incidence of reperfusion arrhythmia, suggesting that it ameliorates reperfusion injury and consequently improves postischemic functional recovery.

Blood cardioplegia in the senescent heart

As an increasingly aged population undergoes cardiac surgery, myocardial protective strategies must address the fundamental differences between adult and senescent myocardium. In a test of the hypothesis that senescent myocardium is less tolerant of cardioplegic arrest, adult (0.5 to 1.0 years) and senescent (6 to 9 years) sheep underwent 55 minutes of hypothermic blood cardioplegic arrest. A 5-minute dose of terminal warm blood cardioplegic solution was administered followed by 30 minutes of vented reperfusion. Left ventricular volume was monitored by means of sonomicrometric crystals in three orthogonal planes. Myocardial function was assessed with the preload recruitable stroke work relationship. Diastolic function was assessed with two techniques: the “stiffness” coefficient ( β ), derived from the exponential end-diastolic pressure-volume relationship, and the time constant of isovolumic left ventricular pressure decay (tau). Data were acquired before arrest and after the reperfusion period. Contractility in the adult hearts was well preserved (preload recruitable stroke work: 63.7 ± 6.1 versus 56.8 ± 4.1 mJ/beat per milliliter per 100 gm, prearrest versus postarrest, p = not significant). In contrast, senescent heart contractility was poorly preserved (56.8 ± 4.1 versus 35.4 ± 4.2 mJ/beat per milliliter per 100 gm, p < 0.025). Early diastolic relaxation (tau) was prolonged in the adult hearts (42.5 ± 3.3 versus 48.8 ± 3.5 msec prearrest versus postarrest, p < 0.05), whereas the senescent hearts were essentially unchanged (49.3 ± 3.1 versus 52.3 ± 4.5 msec, p = 0.35). Myocardial stiffness ( β ) was unchanged in both groups. When compared with adult hearts, contractility in senescent hearts is poorly preserved after cold blood cardioplegic arrest. Active diastolic relaxation, however, is more prolonged in adult hearts. Passive diastolic properties are unchanged in both groups. Because there are specific age-related differences in tolerance to cardioplegic arrest, extrapolation of myocardial protective strategies from studies in adult hearts to elderly patients may not be appropriate. (J T HORAC C ARDIOVASC S URG 1995; 109: 269-74)