Continuous Warm Blood Research Articles

Cardioplegia retrógrada atrial: estudo clínico

This study presents the results in a group of fifteen patients submitted to cardiac surgery, using continuous atrial retrograde warm blood cardioplegia for myocardial protection. Eleven patients were submitted to myocardial revascularization and four were submitted to valvular transplantation. There was no need for inotropic drugs or intraaortic balloon pump support during or after the procedure, and no myocardial infarction was detected in this group. When the heart was arrested, the cardioplegia line was switched to the atrial cannula. The aortic root was vented throughout the cross-clamp period, and retrograde perfusion was assured by noting the engorged exygenated cardiac veins as well as the return of dark blood through the vent in the aortic root. The patients presented good clinical and laboratory course. No right ventricular dysfunction was detected. Two patients were in atrial fibrillation before the surgery, one of them returned to this cardiac rhythm three days after the procedure.

Myocardial Energy Metabolism and Functional Recovery in Coronary Bypass Surgery: A Comparative Study Between Continuous Retrograde Warm and Mild Hypothermic Blood Cardioplegia

The optimal temperature for delivery of continuous retrograde blood cardioplegia is not known. Twenty-two patients admitted to the hospital for elective coronary artery bypass grafting were randomized into the warm (37°) and mild hypothermic (28°C) cardioplegia groups. Changes in myocardial energy metabolism during cardiopulmonary bypass, postoperative efflux of the creatine kinase MB isoform (CK-MB), functional hemodynamic recovery, and postoperative complications were followed. During aortic cross-clamp, the average oxygen consumption was higher in the warm than in the mild hypothermic group (3.4 ± 0.4 vs 2.4 ± 0.3 ml/minute, p = 0.06), as was the average transcardiac (outflow-inflow) pCO2-difference (1.1 ± 0.1 vs 0.7 ± 0.1 kPa, p = 0.02). The average transcardiac pH-difference during aortic cross-clamp was lower in the warm group (−0.08 ± 0.01 vs −0.06 ± 0.01 U, p = 0.02), reflecting more profound tissue acidosis. In accordance with this, warm hearts produced more lactate, especially towards the end of the aortic cross-clamp period (p = 0.001). The net efflux of adenosine and its degradation products was more prominent during warm than during mild hypothermic cardioplegia (p = 0.016), indicating less degradation of high energy adenylates in the hypothermic group. The functional hemodynamic recovery during the first postoperative day was similar in both patient groups, although the myocardial injury estimated as postoperative leakage of CK-MB was less extensive in the hypothermic group (p = 0.011). There were no major differences in the postoperative complications between the study groups. We conclude that continuous retrograde mild hypothermic blood cardioplegia offers better myocardial protection during coronary bypass surgery than does continuous retrograde warm cardioplegia. The clinical significance of this should be tested in a larger series of patients, especially those with recent myocardial infarction, unstable angina, or severely depressed left ventricular function.

Impaired Endothelium-Dependent Relaxation After Cardiac Global Ischemia and Reperfusion: Role of Warm Blood Cardioplegia

Objectives. Experiments were designed to determine whether coronary endothelial dysfunction after cardiac global ischemia and reperfusion could be prevented by warm blood cardioplegic solution.Background. The coronary endothelium produces endothelium-derived relaxing factor (EDRF) to prevent vasospasm and thrombosis. After ischemia and reperfusion, endothelium-dependent relaxation (EDR) is diminished as a result of G-protein dysfunction.Methods. Dogs were exposed to extracorporeal circulation in 37°C (group 1) or 28°C (groups 2 and 3). The heart was ischemic for 120 min while continuous warm blood cardioplegic solution (group 1) or intermittent cold (4°C) crystalloid cardioplegic solution (group 2) was infused into the aortic root. Cardioplegic solution was not used in group 3 animals. The heart was then allowed to function for 60 min of reperfusion.Results. Endothelium-derived relaxation in response to acetylcholine, adenosine diphosphate and sodium fluoride of the coronary rings of group 1 was significantly different from that of groups 2 and 3 but was not significantly different from that of group 4. In contrast, EDR in response to the receptor-independent calcium ionophore agonist A23187 was not significantly different between the four groups. Scanning electron microscopic studies showed that platelet adhesion and aggregation, area of microthrombi, disruption of endothelial cells and separation of the intercellular junction could be found in coronary segments of groups 2 and 3 but not in vessels of groups 1 and 4.Conclusions. These experiments suggest that cardiac global ischemia and reperfusion impair receptor-mediated release of EDRF from the coronary endothelium with G-protein dysfunction. This type of coronary endothelial dysfunction can be prevented by continuous anterograde infusion of warm blood cardioplegic solution during global ischemia.(J Am Coll Cardiol 1997;29:681–7)

術後急性期の心機能におけるＣｏｎｔｉｎｕｏｕｓ ｗａｒｍ ｂｌｏｏｄ ｃａｒｄｉｏｐｌｅｇｉａの優位性

Continuous warm blood cardioplegia (CWBC) の術後急性期の心機能における優位性を cold crystalloid cardioplegia (CCC) を対照して比較検討した. CABG症例をCWBC群 (21例) とCCC群 (15例) に分け, ICU入室時, 1POD, 2PODの心機能, CK, CKMB値と, ICU入室時, 入室後6h, 12h, 18h, 24hのカテコールアミン使用量を測定し比較検討した. 自己心拍再開率はCWBC群が高率だった. 各時点のCIはCWBC群のほうが高値であった. ICU入室時のLVSWI, LVWIもCWBC群で高値であった. RVSWI, RVWIは各時点で両群間に差がなかった. Dopamine, dobutamine 使用量はCWBC群のほうが少なかった. CK, CKMB値はCWBC群のほうが低値であった. これより離脱後心機能や心筋逸脱酵素においてCWBC群のほうがCCC群より優れた結果を示していた.

Effect of intermittent warm blood cardioplegia on functional recovery after prolonged cardiac arrest

There is some evidence that continuous warm blood cardioplegia offers good myocardial protection; however, the effects of interrupting cardioplegia remain controversial. To study this, we compared the effects of continuous and intermittent antegrade warm (37 degrees C) blood cardioplegia on functional recovery after prolonged cardiac arrest (180 minutes). Twenty-four juvenile pigs were randomly assigned into four groups. Group 1 received continuous cardioplegia, group 2 underwent several periods of 15 minutes of cardioplegia interrupted by 5 minutes of normothermic ischemia, and group 3 underwent several periods of 10 minutes of cardioplegia interrupted by episodes of 10 minutes. The hearts of group 4 received no cardioplegia. Left ventricular systolic function was assessed from fractional left ventricular shortening and percentage left ventricular wall thickening, and left ventricular diastolic function was determined from the time constant of relaxation and the constant of myocardial stiffness. Systolic and diastolic functions were slightly depressed 1 and 2 hours after cross-clamp removal in all four groups, without significant differences among the groups. These data suggest that antegrade warm blood cardioplegia can be interrupted for up to 10 minutes without obvious negative effects on left ventricular function in the normal myocardium, provided that the intermittent doses of cardioplegia are sufficient to restore the metabolic demands of the arrested myocardium.

Continuous versus intermittent warm blood cardioplegia: Functional and energetics changes

The aim of this study was to compare the protective effects of continuous warm blood cardioplegia (CWBC) and intermittent warm blood cardioplegia (IWBC) in an experimental model of blood-perfused, isolated rabbit heart. In the CWBC group, cardiac arrest was induced by continuous infusion of blood cardioplegia (10 mEq/L KCl) followed by 30 minutes of reperfusion with blood. In the IWBC group, after 5 minutes of perfusion with blood cardioplegia (10 mEq/L KCl), coronary flow was abolished for 10 minutes, followed by reperfusion with blood cardioplegia for 5 minutes. This sequence was repeated three times for a total period of 45 minutes. Finally the hearts were reperfused for 30 minutes with blood. Infusion of potassium induced a marked increase in coronary perfusion pressure (from 50 +/- 3 to 98 +/- 1 mm Hg; p < 0.01), which remained elevated throughout in the CWBC group, whereas in the IWBC group, it dropped to 0 during each no-flow period. In both groups, cardioplegia resulted in a significant reduction in oxygen consumption (from 5.5 +/- 0.2 to 0.6 +/- 0.03 mL O2.min-1.100 g-1 wet wt; p < 0.01). During CWBC, glucose extraction was significantly reduced (from 152 +/- 10 to 64 +/- 18 micrograms.min-1.g-1 wet wt; p < 0.01). Free fatty acid uptake and creatine kinase and lactate release were not affected. During IWBC, in contrast, a transient but significant release of creatine kinase (from 643 +/- 254 to 2,234 +/- 296 mU.min-1.g-1 wet wt; p < 0.01) and lactate (from 63 +/- 22 to 374 +/- 32 micrograms.min-1.g-1 wet wt; p < 0.01) occurred after each period of ischemia. Despite these metabolic differences, both cardioplegic procedures allowed a prompt and complete recovery of mechanical function and tissue content of high-energy phosphates. Both CWBC and IWBC exert optimal protection in the isolated blood perfused rabbit heart. Thus, IWBC can be safely used to improve visualization of the surgical field.

Continuous warm versus intermittent cold cardioplegic infusion: A comparison of energy metabolism, sodium-potassium adenosine triphosphatase activity, and postischemic functional recovery in the blood-perfused rat heart

We used metabolic, enzymatic, and functional end points to compare the protective properties of continuous warm and intermittent cold cardioplegic infusion in isolated, blood-perfused rat hearts. After excision, hearts ( n = 12 per group) were preserved for 3 hours by one of the following cardioplegic procedures: (1) continuous infusion of warm (37º C) blood cardioplegic solution prepared by mixing Fremes' solution with rat arterial blood in a ratio of 1:4, (2) continuous infusion of warm (37º C) crystalloid cardioplegic solution prepared by mixing Fremes' solution with bicarbonate buffer solution in a ratio of 1:4, or (3) intermittent infusion of cold (20º C) St. Thomas' Hospital cardioplegic solution number 2 infused for 3 minutes every 30 minutes during a 3-hour period of ischemia. In the continuous-infusion cardioplegic groups, the solution was infused through the aorta at a flow rate of 0.8 ml · min -1 · gm -1 heart. At the end of the 3-hour preservation period, myocardial sodium-potassium adenosine triphosphatase activity (an index of ion-exchange activity) was assessed in six hearts in each group. The remaining hearts in each group were then aerobically perfused at 37º C with arterial blood (from a support rat) for a further 50 minutes, during which time they were atrially paced at 320 beats/min. At the end of this period, left ventricular developed and end-diastolic pressures were assessed with an intraventricular balloon; the hearts were then freeze-clamped and taken for the measurement of tissue adenosine triphosphate and creatine phosphate content. Hearts ( n = 6) aerobically perfused with blood for 50 minutes (no cardioplegic infusion) served as control preparations. At a balloon volume of 180 μl, the mean final values for left ventricular developed pressure in the continuous warm blood, continuous warm crystalloid, and intermittent cold cardioplegic groups were 98 ± 5 mm Hg ( p < 0.05), 70 ± 5 mm Hg, and 78 ± 5 mm Hg, respectively. This was compared with 122 ± 5 mm Hg in control hearts ( p < 0.05 vs the rest). For left ventricular end-diastolic pressure, the corresponding values were 33 ± 3 mm Hg, 32 ± 6 mm Hg, and 14 ± 4 mm Hg ( p < 0.05), respectively. The control value was 16 ± 3 mm Hg ( p < 0.05 vs continuous warm blood and continuous warm crystalloid groups). Tissue content of adenosine triphosphate was similarly reduced to approximately 50% of control values in all groups, and creatine phosphate content fully recovered in all groups. Sodium-potassium adenosine triphosphatase activity was poorly preserved in continuous warm crystalloid–treated hearts (0.012 ± 0.003 vs 0.030 ± 0.008 μmol inorganic phosphate · mg -1 · min -1 in control preparations, p < 0.05), whereas in continuous warm blood and intermittent cold cardioplegic groups (0.032 ± 0.015 and 0.031 ± 0.013 μmol inorganic phosphate · mg -1 · min -1) there was no significant loss of activity. In conclusion, (1) none of the procedures conferred complete protection, (2) continuous warm blood cardioplegic infusion provided superior preservation of systolic function and intermittent cold cardioplegic infusion afforded superior protection with respect to diastolic function, and (3) both continuous warm blood and intermittent cold cardioplegic infusion similarly protected sodium-potassium adenosine triphosphatase activity and tissue adenosine triphosphate and creatine phosphate content, whereas continuous warm crystalloid cardioplegic infusion afforded poor preservation of sodium-potassium adenosine triphosphatase activity. In general, the poorest protection was afforded by continuous warm crystalloid cardioplegic infusion. (J T HORAC C ARDIOVASC S URG 1996;112:797-805)

Continuous warm blood cardioplegia: A randomized prospective clinical comparison

Seventy-eight patients undergoing isolated coronary artery bypass grafting (CABG) were randomized to receive one of two myocardial preservation techniques. Control patients (C) (n = 38) had myocardial protection by moderate systemic hypothermia, topical cold saline, and myocardial arrest with antegrade dilute blood/cold potassium cardioplegia with subsequent intermittent retrograde solution every 10–15 minutes during the period of aortic cross-clamping. The experimental group (warm blood, WB) (n = 40) had myocardial protection at systemic normothermia, myocardial arrest with antegrade high potassium, and warm blood cardioplegia with subsequent continuous retrograde low potassium warm blood cardioplegia throughout aortic cross-clamping. The two groups were similar preoperatively. After aortic declamping, all WB patients developed a spontaneous rhythm. Only three (7.5%) required intraoperative defibrillation compared with 23 (61%) C patients,p <0.0001. The cross-clamp time per graft was greater with WB,p = 0.003. The postoperative need for inotropes, cardiac pacing, incidence of ventricular dysrhythmia, chest tube drainage, and hospital stay did not differ between groups. Perioperative myocardial infarction occurred in 2 WB and 0 C patients (p = 0.25). Mortality was not different between groups (WB = 1, C = 2,p = 0.89). It is possible to perform CABG with continuous warm blood cardioplegia with low morbidity and mortality. However, no clear advantage was demonstrated over standard techniques that allow the technical ease of a bloodless field. The metabolic and physiologic significance of spontaneous resumption of sinus rhythm upon aortic declamping remains to be elucidated.

Troponin T release with warm and cold cardioplegia.

Cardiac troponin T (cTnT) levels were measured in 41 patients undergoing elective coronary artery surgery. Twenty-one patients received continuous warm antegrade blood cardioplegia to maintain asystole whilst 20 patients received antegrade cold blood cardioplegia intermittently. Serum levels of cTnT were determined preoperatively and at 0, 6, 12 and 18 h postbypass. Peak cTnT levels and total cTnT release (calculated from the area under the curve postoperatively) were found to be significantly higher (p < 0.05: Mann-Whitney) when cold cardioplegic solutions were used. Continuous warm cardioplegia results in lower cTnT release than intermittent cold blood cardioplegia suggesting that the former may provide better myocardial preservation.

Changes in atrial natriuretic factor (ANF) and Ca+2 ATPase mRNA transcriptional activity are markers of myocardial integrity during continuous warm blood cardioplegia (CWBCP) in rats.

Annals of the New York Academy of SciencesVolume 793, Issue 1 p. 419-422 Changes in Atrial Natriuretic Factor (ANF) and Ca++ ATPase mRNA Transcriptional Activity Are Markers of Myocardial Integrity during Continuous Warm Blood Cardioplegia (CWBCP) in Rats E. S. REMSEY, E. S. REMSEY Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorM. A. BAIG, M. A. BAIG Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorJ. G. KRAL, Corresponding Author J. G. KRAL Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203b Corresponding author.Search for more papers by this authorK. D. EGHBALI, K. D. EGHBALI Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorM. VARGA, M. VARGA Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorR. B. WAIT, R. B. WAIT Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorM. A. Q. SIDDIQUI, M. A. Q. SIDDIQUI Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this author E. S. REMSEY, E. S. REMSEY Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorM. A. BAIG, M. A. BAIG Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorJ. G. KRAL, Corresponding Author J. G. KRAL Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203b Corresponding author.Search for more papers by this authorK. D. EGHBALI, K. D. EGHBALI Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorM. VARGA, M. VARGA Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorR. B. WAIT, R. B. WAIT Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this authorM. A. Q. SIDDIQUI, M. A. Q. SIDDIQUI Department of Surgery and aDepartment of Anatomy and Cell Biology State University of New York Health Science Center at Brooklyn Box 40 450 Clarkson Avenue Brooklyn, New York 11203Search for more papers by this author First published: September 1996 https://doi.org/10.1111/j.1749-6632.1996.tb33533.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Volume793, Issue1Myocardial Preservation, Preconditioning, and Cellular AdaptationSeptember 1996Pages 419-422 RelatedInformation

Antegrade and retrograde continuous warm blood cardioplegia: A 31P magnetic resonance study

Retrograde normothermic blood cardioplegia has been shown to provide myocardial protection during certain bypass procedures. However, a number of animal studies have shown less than optimal myocardial protection with this technique. Isolated, beating porcine hearts were perfused antegradely (aortic root pressure = 75 to 95 mm Hg) for 30 minutes. Arrest was induced and maintained for 60 minutes with high K+ blood cardioplegia delivered either antegradely (n = 8) or retrogradely (n = 8) (coronary sinus pressure = 35 to 55 mm Hg). Perfusate was switched to normokalemic blood for recovery of sinus rhythm (30 minutes). Intracellular pH, creatine phosphate, inorganic phosphate, and adenosine triphosphate were monitored continuously and noninvasively with phosphorus 31 magnetic resonance spectroscopy throughout the experiment, and functional variables (rate-pressure product and the positive and negative first derivatives of left ventricular pressure) were assessed concurrently. Antegrade cardioplegia maintained high-energy metabolites, intracellular pH, and myocardial function. Retrograde normothermic blood cardioplegia resulted in an increase in inorganic phosphate (197% +/- 15% of control) and a decrease in creatine phosphate (51% +/- 6% of control). There was no significant difference in myocardial function between the two groups (p > 0.05). The magnetic resonance spectroscopy data indicate ischemia occurred within 2 minutes of the initiation of retrograde perfusion. This study suggests that retrograde normothermic blood cardioplegia causes a transition of the myocardium to ischemic metabolism in the normal porcine heart.

Ultrastructural changes during continuous retrograde warm and mild hypothermic blood cardioplegia for coronary bypass operations

Ultrastructural changes in myocardial tissue were studied in 21 patients undergoing elective aorta-coronary bypass operation. The patients were randomized into two groups, with 10 of them receiving continuous retrograde warm and 11 continuous retrograde mild hypothermic blood cardioplegia. Biopsy specimens for electron microscopy were taken from the apical part of the left ventricle before and at the end of the aortic crossclamp period and after reperfusion of the myocardium. The ultrastructural changes were analyzed with use of a semiquantitative scoring system and classified as mild, moderate, or severe. Slight ultrastructural changes were found in both groups even before the aortic crossclamp period. At the end of the aortic crossclamp period the most prominent ultrastructural changes were mitochondrial swelling, damage of capillary endothelium, and clearing of the nucleoplasm or margination of chromatin, but some enlargement in intercalated discs was also discernible. Reperfusion of the myocardium for 15 minutes somewhat further increased the overall score of the ultrastructural changes. Two patients in the warm cardioplegia group had a perioperative myocardial infarction, and this may be one reason for the higher postoperative creatine kinase MB efflux in this patient group. Despite this finding, no major differences in the ultrastructural changes between the two cardioplegia groups could be observed. We conclude that only mild to moderate and principally reversible ultrastructural changes occur in myocardium during continuous retrograde warm and mild hypothermic blood cardioplegia for coronary bypass operation.

A 31P-Nuclear magnetic resonance study of intermittent warm blood cardioplegia

This study was designed to assess the effects of intermittent warm blood cardioplegia on myocardial energy metabolites, intracellular pH, and contractile function. The isolated blood-perfused pig hearts were divided into three groups. After 30 minutes of control perfusion, the hearts in group 1 ( n = 10) received 90 minutes of continuous warm (37° C) blood cardioplegia; the hearts in group 2 ( n = 9) received six 5-minute periods of warm blood cardioplegia, interrupted by six 10-minute episodes of ischemia (37° C). The hearts were then reperfused for 30 minutes. The hearts in group 3 underwent 150 minutes of control perfusion without cardioplegia or ischemic episodes. Phosphorus 31-nuclear magnetic resonance spectra showed that a 10-minute interruption of warm blood cardioplegia decreased phosphocreatine levels and intracellular pH by approximately 47% ( p < 0.01) and 0.12 unit ( p < 0.05), respectively, and increased inorganic phosphate levels by approximately 87%, whereas resumption of cardioplegia for 5 minutes resulted in almost 100% recovery of phosphocreatine and inorganic phosphate levels and intracellular pH. More important, subsequent interruptions did not result in any cumulative changes in phosphocreatine level, inorganic phosphate level, or intracellular pH beyond those changes observed after the initial cardioplegic interruption. Moreover, during reperfusion there were no significant differences in adenosine triphosphate and phosphocreatine levels among the three groups of hearts. Furthermore, hearts from groups 1 and 2 showed comparable recovery of contractile function. These results indicate that six 10-minute interruptions and six 5-minute restorations of warm blood cardioplegia caused only mild and reversible changes in myocardial energy metabolites and intracellular pH and these changes were not cumulative. This study suggests that antegrade intermittent warm blood cardioplegia may provide as much myocardial protection as does antegrade continuous warm blood cardioplegia in the normal heart . (J T HORAC C ARDIOVASC S URG 1995;109:1155-63)

Retrograde cardioplegia does not adequately perfuse the right ventricle

Surgeons often rely primarily on retrograde cardioplegia for myocardial protection, because it provides adequate left ventricular perfusion even in the presence of coronary artery disease. Clinically, however, adequate right ventricular perfusion by retrograde delivery has not been demonstrated. Using intraoperative transesophageal echocardiography, we examined retrograde delivery of cardioplegic solutions by contrast echocardiography, which directly assesses myocardial perfusion. In 15 patients (seven having coronary bypass and eight having valve operations), 4 ml of sonicated Isovue medium was injected retrograde via a coronary sinus catheter. Myocardial perfusion was assessed quantitatively by visual inspection and background-subtracted videodensitometric analysis. In five patients undergoing aortic valve replacement, right and left coronary ostial drainage was estimated during retrograde infusion. Before the aortic crossclamp was removed, myocardial oxygen extraction was calculated in all 15 patients by first delivering warm blood cardioplegic solution for 2 minutes in a retrograde fashion and then taking samples from the cardioplegia line and aortic root. This determined the oxygen extraction ratio across the myocardium at the end of retrograde delivery. Warm blood cardioplegic solution was next given antegrade, and 15 seconds later samples were taken from the cardioplegia line and a right ventricular (acute marginal) vein to determine the oxygen extraction ratio across the right ventricle. As assessed by contrast echocardiography, retrograde infusion resulted in almost four times more perfusion to the left ventricular free wall and septum than to the right ventricular free wall (74 ± 2 versus 69 ± 2 versus 20 ± 2, p < 0.05). In those five patients with an aortotomy the right ostial drainage was less than 5 ml/min whereas left ostial drainage was estimated at 80 ml/min during retrograde administration. Oxygen extraction across the myocardium supplied by retrograde infusion was low after 2 minutes. Conversely, when antegrade cardioplegia was started, right ventricular oxygen extraction rose fourfold (42% ± 5% versus 11% ± 1%, p < 0.05), demonstrating that retrograde cardioplegia had not adequately perfused the right ventricular myocardium. Conclusions: 1. Retrograde cardioplegia provides poor right ventricular myocardial perfusion as assessed by contrast echocardiography and coronary ostial drainage. 2. This poor perfusion is inadequate to meet myocardial demands as demonstrated by the high right ventricular oxygen extraction after a prolonged retrograde infusion. 3. Therefore surgeons must not rely solely on retrograde cardioplegia for right ventricular myocardial protection. This concept is especially important if continuous warm blood cardioplegia is used, because myocardial requirements are then higher. (J T HORAC C ARDIOVASC S URG 1995;109:1116-26)

Warm heart surgery in cold haemagglutinin disease

Continuous warm retrograde blood cardioplegia and systemic normothermia are a promising method for heart surgery in patients with cold autoimmune disorders in order to avoid the adverse effects of both systemic and coronary hypothermia during cardiac arrest and cardiopulmonary bypass. A 59-year-old white man with cold haemagglutinin disease who underwent coronary surgery using continuous retrograde normothermic blood cardioplegia and systemic normothermia is reported.

Warm Heart Surgery in Cold Haemagglutinin Disease

Continuous warm retrograde blood cardioplegia and systemic normothermia are a promising method for heart surgery in patients with cold autoimmune disorders in order to avoid the adverse effects of both systemic and coronary hypothermia during cardiac arrest and cardiopulmonary bypass. A 59-year-old white man with cold haemagglutinin disease who underwent coronary surgery using continuous retrograde normothermic blood cardioplegia and systemic normothermia is reported.

Experience with warm blood cardioplegia in 480 patients

From 1 March 1992 too 31 July 1993 (17 months), 480 consecutive patients underwent various open-heart procedures under anterograde (83 patients) or retrograde (397 patients) continuous warm blood cardioplegia. Some 352 patients (73.3%) had isolated coronary artery bypass grafts (CABG) and 117 (24.3%) had valve replacement either isolated (96) or in combination with other operations (21). Two patients had CABG and ventricular aneurysmectomy, eight had correction of congenital defects, and one had resection of left atrial myxoma. The 30-day postoperative mortality rate was 2.9% (14 deaths). In four patients the cause of death was not cardiogenic. An intra-aortic balloon was used in 11 patients following CABG (3.1%) with six survivors. Perforation of the coronary sinus occurred in one patient. Perioperative myocardial infarction was observed in 5.6% of patients after CABG. No myocardial infarction occurred after valve replacement. Phrenic nerve injury and wound infection were not observed. These results indicate that warm blood cardioplegia, especially when delivered retrogradely, provides excellent myocardial protection of both ventricles during various open-heart procedures.

Experience with Warm Blood Cardioplegia in 480 Patients

From 1 March 1992 too 31 July 1993 (17 months), 480 consecutive patients underwent various open-heart procedures under anterograde (83 patients) or retrograde (397 patients) continuous warm blood cardioplegia. Some 352 patients (73.3%) had isolated coronary artery bypass grafts (CABG) and 117 (24.3%) had valve replacement either isolated (96) or in combination with other operations (21). Two patients had CABG and ventricular aneurysmectomy, eight had correction of congenital defects, and one had resection of left atrial myxoma. The 30-day postoperative mortality rate was 2.9% (14 deaths). In four patients the cause of death was not cardiogenic. An intra-aortic balloon was used in 11 patients following CABG (3.1%) with six survivors. Perforation of the coronary sinus occurred in one patient. Perioperative myocardial infarction was observed in 5.6% of patients after CABG. No myocardial infarction occurred after valve replacement. Phrenic nerve Injury and wound infection were not observed. These results indicate that warm blood cardioplegia, especially when delivered retrogradely, provides excellent myocardial protection of both ventricles during various open-heart procedures.

Effects of magnesium on myocardial function after coronary artery bypass grafting

The effects of perioperative administration of magnesium sulfate on myocardial function was studied in patients with unstable angina (grade IV) undergoing coronary artery bypass grafting. Myocardial protection consisted of antegrade and retrograde continuous warm blood cardioplegia. Patients were randomly divided into two groups. Group A (50 patients) received intravenous magnesium sulfate (16 mmol) continuously from the time of anesthetic induction to aortic cross-clamping and a second dose (32 mmol) starting after the release of aortic cross-clamp until 24 hours later. Group B (48 patients) did not receive magnesium sulfate and served as control. Left ventricular stroke work index increased in group A from 34 +/- 3 g.m/m2 before operation to 42 +/- 3 g.m/m2, 45 +/- 2 g.m/m2, and 47 +/- 2 g.m/m2, 1, 6, and 12 hours after operation, respectively (p < 0.05 versus preoperative), and in group B from 33 +/- 3 g.m/m2 before operation to 38 +/- 3 g.m/m2, 40 +/- 2 g.m/m2, and 41 +/- 2 g.m/m2, 1, 6, and 12 hours after operation, respectively (p < 0.05). Left ventricular stroke work index was higher in group A 6 (p = 0.06), 12, and 24 hours (p < 0.05) after operation compared with group B. The incidence of ventricular arrhythmias requiring treatment was significantly higher (p < 0.05) in group B: 14 patients versus 1 patient in group A. Postoperative hypertension was more frequent in group B: 16 patients versus 2 patients in group A (p < 0.05). These results indicate that perioperative administration of magnesium sulfate may contribute to better myocardial recovery and fewer ventricular tachyarrhythmias after operation.

The failure of retrograde continuous warm-blood cardioplegia to resuscitate cardiac function in experimental acute coronary artery occlusion and reperfusion.

The effects of retrograde continuous warm-blood cardioplegia (RCWBC) on myocardial preservation during surgical revascularization for acute coronary artery occlusion were investigated using an isolated in-situ dog heart model. The left anterior descending artery (LAD) was occluded for 60 minutes followed by 60 minutes of cardioplegic arrest and reperfusion after release of the coronary artery occlusion. Thirty one animals were divided into 3 groups according to the manner of cardioplegic arrest. The first group of animals (n=10) received multiple doses of cold St. Thomas' Hospital solution delivered antegradely through the aortic root. The second group of animals (n=11) received the same dose of the crystalloid solution delivered retrogradely through the coronary sinus. The third group of animals (n=10) received RCWBC through the coronary sinus. In the animals which were capable of supporting the working mode after reperfusion (8 hearts in each group), regional myocardial function in the occluded LAD distribution measured by sonomicrometer as well as global myocardial function evaluated by left-ventricular stroke-work index were not significantly improved during reperfusion by RCWBC. Corresponding to the functional data, myocardial pH in the occluded LAD distribution was not significantly increased by RCWBC. Although RCWBC maintained myocardial pH in the circumflex artery distribution at a significantly higher level than the other two groups of hearts undergoing cold crystalloid cardioplegia, RCWBC resulted in a substantial decline of myocardial pH in the right-ventricular free wall. These results suggest that RCWBC after 60 minutes of LAD occlusion may not provide a significant benefit in myocardial preservation compared to cold crystalloid cardioplegia delivered through either an antegrade or retrograde manner.