First report of intramyocardial pH in man. II. Assessment of adequacy of myocardial preservation

Intramyocardial pH and temperature were continuously measured in the anteroseptal region in 40 patients undergoing aortic cross-clamping during cardiac operations. Myocardial protection was achieved with systemic cooling (25 degrees C) and multidose potassium cardioplegia (4 degrees C). A clinical myocardial preservation score was devised based on intraoperative and postoperative need for inotropic support, postoperative creatine kinase isoenzyme (CK-MB) and electrocardiographic changes, and radionuclide ventriculography. The patients were divided into three groups according to their preservation scores. Group I (n = 17) with good preservation (scores 0 to 2), Group II (n = 15) with fair preservation (scores 3 to 8), and Group III (n = 8) with poor preservation (scores 9 to 15). Baseline intramyocardial pH was similar in all groups (mean +/- SEM = 6.77 +/- 0.03). With the administration of cold potassium cardioplegia, intramyocardial pH rose above baseline in all three groups. The magnitude of this rise related directly to the adequacy of preservation and to the duration of the cross-clamp period. Patients with lowest preservation scores and shortest cross-clamp periods had the highest intramyocardial pH. In contrast, there was no relationship between myocardial temperature during cross-clamp and either intramyocardial pH or the preservation score. The integrated mean intramyocardial pH during cross-clamp was found to be the parameter that correlated most with the adequacy of preservation. The correlation between intramyocardial pH and myocardial temperature during the period of cross-clamping related to the length of this period; it was good (r = 0.76, p less than 0.01) in periods of 40 minutes or less and very poor in periods exceeding 60 minutes (r = 0.27, p greater than 0.10). It is concluded that (1) the magnitude of rise in intramyocardial pH during the period of aortic cross-clamping is a good indicator of the adequacy of myocardial preservation; (2) during periods of aortic cross-clamping exceeding 40 minutes, myocardial temperature is a poor indicator of adequacy of preservation, since progressive tissue acidosis may occur despite low myocardial temperatures; and (3) techniques and solutions that can effectively reduce the progression of tissue acidosis will, in most likelihood, enhance our ability to protect the ischemic myocardium during cardioplegic arrest.     

Comparison of alternative cardioplegic techniques

Cold potassium cardioplegia provides adequate protection for coronary bypass operations, but severe coronary stenoses limit cardioplegic delivery to ischemic regions. The traditional technique delivers cardioplegic solution into the aortic root during the performance of distal anastomoses. The proposed alternative technique constructs proximal as well as distal anastomoses during a prolonged cross-clamp period, but permits more uniform cooling. The two techniques were compared in a prospective concurrent trial of 45 patients undergoing elective coronary bypass grafting. The traditional technique was employed in 26 patients (Group A) and the alternative technique in 19 patients (Group B). In both groups, 700 to 1,000 ml of a crystalloid cardioplegic solution was infused into the aortic root after application of the aortic cross-clamp. In Group A (traditional technique), 500 ml was infused into the aortic root after each distal anastomosis. In Group B (alternative technique), cardioplegic solution was administered through the vein graft after each distal anastomosis, and a proximal anastomosis was constructed after distal anastomoses to the most ischemic regions to permit continued cardioplegic delivery to these regions. The cross-clamp period was shorter in Group A than in Group B (44 +/- 15 versus 60 +/- 18 minutes, p less than 0.01), but the mean temperature in the most ischemic region was warmer (Group A, 19 degrees +/- 3 degrees C; Group B, 15 degrees +/- 3 degrees C, p less than 0.05). The postoperative CK-MB was higher in Group A (Group A, 47 +/- 36; Group B, 21 +/- 9 IU/L, p less than 0.01). Cardiac lactate production persisted longer in Group A (Group A, 4 +/- 1; Group B, 1 +/- 1 hours postoperatively, p less than 0.05). Volume loading 4 hours postoperatively produced a similar increase in left atrial pressure and cardiac index in both groups. In response to volume loading, Group A patients produced lactate, but Group B patients extracted lactate (change in cardiac lactate extraction: Group A, -1.7 +/- 2.3; Group B, +2.5 +/- 5.1 mg/dl, p less than 0.05). The construction of proximal as well as distal anastomoses during a prolonged cross-clamp period permits more uniform cooling and immediate reperfusion. This alternative technique resulted in less injury (CK-MB release) and more rapid recovery of myocardial metabolism.     

Myocardial protection by intermittent perfusion with cardioplegic solution versus intermittent coronary perfusion with cold blood

The myocardial protection provided by cardioplegic solution using buffered, isosmotic potassium (30 mEq. per liter) was compared with intermittent cold coronary perfusion for 2 hours of aortic cross-clamping in dogs. The cardioplegic solution (Group CS) or cold blood (Group CB) was infused every 15 minutes through a cooling coil to reduce the perfusate temperature to 5 degrees C. Myocardial function after 30 minutes of reperfusion and rewarming was reduced in Group CB with a significant reduction in peak systolic pressure at a left ventricular (LV) balloon volume of 20 ml. and a significant reduction of dp/dt. In contrast, in Group CS, LV function was unchanged from the base-line period. LV compliance also was significantly reduced in Group CB while being unchanged in Group CS. Myocardial extravascular water content, obtained by dessication, was significantly higher in Group CB than in Group CS, which may explain the reduction in compliance. Electron microscopy showed normal ultrastructure in Group CS but extracellular edema in Group CB. Total coronary blood flow showed a sustained increase during reperfusion in both groups. Oxygen consumption rose with rewarming to base-line levels in both groups, whereas lactate and pyruvate consumption was reduced in both groups, particularly Group CB. Cardioplegic solution thus appears to be superior to the intermittent perfusion of cold blood for myocardial protection. The addition of potassium arrest, by markedly reducing myocardial metabolism, improves the protection afforded by cold blood perfusion alone.     

The importance of monitoring intramyocardial temperature during hypothermic myocardial protection.

In 50 patients undergoing cardiac operation, hypothermic cardioplegic solution was infused into the root of the aorta immediately after aortic cross-clamping. Cardiac standstill was achieved within 1 to 3 minutes. However, monitoring of intramyocardial temperature with a needle thermistor revealed that such core cooling is unpredictable (the intramyocardial temperature achieved ranged from 7 degrees to 33 degrees C), unstable (this temperature can rise at more than 0.5 degrees C per minute), and uneven (a difference of up to 17 degrees C was observed between the intramyocardial temperature of the anterior and posterior left ventricular sites). The area supplied by the stenotic coronary artery was least protected. Monitoring of intramyocardial temperature enables one to know when supplementary cooling is indicated. We conclude that widespread differences in this temperature during cardiac operation make monitoring advisable for optimal myocardial protection.     

Right ventricular function in retrograde cardioplegia for myocardial protection--an experimental study

Anterior cardiac veins which are the main drainage vessels of the right ventricle drain directly into the right atrium. Therefore, the right ventricular wall may not be perfused effectively during open heart surgery by the use of retrograde cardioplegic method resulting in postoperative right ventricular dysfunction. Seventeen mongrel dogs were subjected to this study and were placed on cardiopulmonary bypass using a conventional heart-lung machine. Total aortic cross-clamping time was 60 minutes in all dogs. In Group I (n = 6), 4 degrees C St. Thomas' Hospital solution (15 ml/kg body weight) was injected into the aortic root by the use of a syringe. Cardioplegic solution was replenished every 20 minutes with a half of the initial dose (7.5 ml/kg body weight). Group II (n = 6) were the dogs with the retrograde cardioplegia in which 4 degrees C St. Thomas' Hospital solution (15 ml/kg body weight) was given retrogradely from the coronary sinus by the drip method at the height of 60 cm, and the replenishing dose and interval of cardioplegia were the same as Group I. Group III (n = 5) was the dogs treated with retrograde cardioplegia identical to Group II and the combined use of topical cooling with ice-slush. The hearts were resuscitated after 60 minutes of aortic cross-clamping. Right ventricular functions such as cardiac output, right atrial pressure, right ventricular end-diastolic pressure, right ventricular max dp/dt, and shortening fraction of the right ventricle were measured 15, 30, 45, and 60 minutes after cardiac resuscitation respectively. In Group II, right atrial pressure was significantly elevated from the control value 15 and 30 minutes after cardiac resuscitation. On the other hand, all indices of right ventricular functions in Group III showed insignificant changes. The present experimental study demonstrated the retrograde cardioplegic method could produce right ventricular perfusion resulting in right ventricular dysfunction early after cardiac resuscitation. This deleterious effect however could be prevented by the combined use of topical cooling of the right ventricle with ice-slush.     

Cardioplegic arrest and intermittent aortic clamping: comparison in coronary artery bypass graft

427 randomized patients undergoing coronary artery bypass graft (CABG) were divided into two groups. In Group A (269 patients), myocardial protection was achieved using cardioplegic solution (Bretschneider). Group B (158 patients) was operated with intermittent aortic cross-clamping. Between both groups there was no significant difference in early postoperative mortality rates, incidence of postoperative low output syndrome, perioperative myocardial infarctions, length of ICU-stay, length of intubation, incidence of arrhythmia, and inotropic requirements. The ratio of reperfusion time divided by aortic cross-clamping time (R/C-ratio) in Group B (1.06 + 1.17) was larger than in Group A (0.49 + 0.17), which could explain this result. In Group A significantly larger incidence of postoperative arrhythmia was recognized, if reperfusion time was shorter than 20 minutes. Also in Group A, longer postoperative intubation was required with R/C-ratio under 0.60. In Group B longer intubation was needed postoperatively with aortic cross-clamping time longer than 30 minutes, reperfusion time shorter than 30 minutes, or R/C-ratio under 0.80. In conclusion, reperfusion should be continued at least for 20 minutes and if possible, for the length equivalent to R/C-ratio over 0.60 in CABG with presently widely used cardioplegic arrest.     

Verapamil and myocardial preservation in patients undergoing coronary artery bypass surgery

The value of verapamil hydrochloride as a myocardial preservative when administered prior to or during periods of myocardial ischemia was studied in patients with normal preoperative cardiac function during elective coronary artery bypass grafting. Myocardial protection included systemic hypothermia (28 degrees C) and hypothermic hyperkalemic cardioplegia. Patients were randomly divided into four groups. Group 1 received intravenous administration of verapamil prior to aortic cross-clamping. Group 2 received intravenous verapamil plus verapamil in the cardioplegic solution. Group 3 received verapamil in the cardioplegic solution only. Group 4 was given no verapamil. Oxygen extraction during the reperfusion period was greatest in Group 4. However, the incidence of pacing was 50 to 78% in Groups 2 and 3, who were given verapamil in the cardioplegic solution. These groups also had a greater need for inotropic agents for discontinuation of cardiopulmonary bypass (CPB). This study indicates that verapamil may be a useful pretreatment prior to CPB and ischemia, but is not effective and may even be detrimental when administered during ischemic periods to patients with good myocardial function.     

Reduction of myocardial injury with verapamil before aortic cross-clamping

The effect of verapamil administered before aortic cross-clamping was assessed in 40 patients undergoing elective coronary artery bypass grafting. Myocardial protection consisted of cold blood potassium cardioplegia, topical ice slush, and moderate (28 degrees C) systemic hypothermia. Patients were randomly divided into two groups: group 1 (18 patients) received verapamil (0.1 mg/kg up to 10 mg) intravenously three to five minutes before aortic cross-clamping; group 2 (22 patients) did not (control). Myocardial injury was assessed by cumulative release of the cardiac-specific isoenzyme of creatine kinase (CK-MB) after release of the aortic cross-clamp. Release of CK-MB was significantly lower in the verapamil group (44.9 +/- 6.2 versus 72.2 +/- 9.0 IU at 24.5 hours, p = 0.005). Calculated total infarct size was also lower in the verapamil group (6.0 +/- 0.9 versus 8.9 +/- 1.0 g-Eq, p = 0.035). Individual CK-MB release curves showed either one or two peaks. The two-peak pattern was more frequent in control patients (18 of 21 control patients versus 6 of 18 verapamil patients, p = 0.001) and was associated with a larger infarct size. Atrioventricular pacing was not required in any verapamil patient, but was needed in 1 control patient. We conclude that verapamil administered before aortic cross-clamping protects against myocardial injury during coronary artery bypass grafting with no increase in the incidence of atrioventricular block.     

Clinical study of blood cardioplegia--for aerobic metabolism during aortic cross-clamping

Blood cardioplegia is considered to be superior in oxygenating potential, buffering potential, oncotic, and other physiologic effects. In clinical cases, however, it is unproven whether aerobic metabolism can be obtained by using blood cardioplegia during aortic cross-clamping. Aerobic metabolism during aortic cross-clamping was therefore evaluated in patients with valvular heart disease who underwent relatively long periods of ischemic arrest. Myocardial metabolism of oxygen, lactate and pyruvate was studied in 14 patients under 126 +/- 41.2 min of cardiac arrest, and intramyocardial carbon dioxide tension (PmCO2) was also monitored continuously in 23 patients who received 121 +/- 29.8 min of aortic cross-clamping. After aortic cross-clamping, 4 degrees C St. Thomas solution was infused for immediate cooling, followed by blood cardioplegia for replenishment every 20-25 min. Blood cardioplegia and myocardial temperature were maintained within 15-20 degrees C by using an automatic cardiac hypothermia control system. Myocardial oxygen extraction during the pre-ischemic period was 26.8 +/- 13.3%. At 15 and 30 min after reperfusion, it was 30.0 +/- 10.8% and 33.8 +/- 8.2%, respectively. During ischemic arrest, myocardial oxygen extraction decreased, but the infusion of blood cardioplegia kept it above 14.0 +/- 9.3% at all times. As for lactate metabolism, although some cases showed lactate production even before the aortic cross-clamping, lactate extraction was attained in some cases during blood cardioplegia perfusion. Changes in excess lactate and redox potential of lactate and pyruvate (delta Eh) showed that aerobic metabolism could be obtained in 13/32 (41%) infusions of blood cardioplegia. PmCO2 at the aortic cross-clamp was 47.0 +/- 27.7 mmHg, and gradually rose during the ischemic arrest, but only as far as 68.4 +/- 64.8 mmHg at the time of cross-clamp release. PmCO2 decreased with each infusion of blood cardioplegia, and the decrease lasted up to 10 minutes. Though PmCO2 began to rise thereafter, the effect of blood cardioplegia continued as long as 20-25 min after the infusion. In conclusion, blood cardioplegia provides aerobic metabolism during aortic cross-clamping even in clinical setting, provided that cardiac hypothermia and delivery of cardioplegic solution are maintained appropriately.     

Cold blood as the vehicle for potassium cardioplegia

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.     

Comparison of myocardial temperatures with multidose cardioplegia versus single-dose cardioplegia and myocardial surface cooling during coronary artery bypass grafting

Myocardial hypothermia with multidose cardioplegia has not been compared with single-dose cardioplegia and myocardial surface cooling with a cooling jacket in patients having coronary artery bypass grafting. In this study, 20 patients with three-vessel disease undergoing coronary bypass at 28 degrees C with bicaval cannulation, caval tapes, and pulmonary artery venting (4.9 +/- 0.7 grafts per patient) were prospectively randomized equally into group I (multidose cardioplegia) and group II (single-dose cardioplegia with a cooling jacket). The initial dose of cardioplegic solution was 1000 ml. Group I then received 500 ml of cardioplegic solution every 20 minutes, delivered into the aortic root and available grafts. In group II, after the cardioplegic solution had been administered, a cooling jacket covering the right and left ventricles was applied. In both groups temperatures were recorded every 30 seconds at five ventricular sites: (1) right ventricular epicardium; (2) right ventricular myocardium or cavity, 7 mm; (3) left ventricular epicardium; (4) left ventricular myocardium or cavity, 15 mm; and (5) septum, 20 mm. Group mean temperatures at each site at various times were compared within each group and between the two groups by analysis of variance. Aortic crossclamp time was 60.3 +/- 12.1 minutes in group I and 52.8 +/- 7.3 minutes in group II (p = 0.12); cardiopulmonary bypass time was 103.7 +/- 11.1 minutes in group I versus 87.7 +/- 12.7 minutes in group II (p less than 0.01). One minute after the cardioplegic solution was initially given, temperatures between groups at each site were not statistically different, but left ventricular epicardial temperatures within both groups were significantly higher than in the other four sites. Nineteen minutes after administration of the cardioplegic solution, temperatures in group I at all sites were higher than in group II. Similarly, throughout the entire period of aortic crossclamping, mean temperatures (except left ventricular myocardial site), maximum temperatures, and percentage of time all temperatures were 15 degrees C or higher were greater in group I than in group II. The following conclusions can be reached: 1. Initial myocardial cooling with 1000 ml of cardioplegic solution is not significantly limited by coronary artery disease but is suboptimal (16 degrees or 17 degrees C) in the inferior left ventricular epicardium because of continual warming from the aorta and subdiaphragmatic viscera. 2. Without myocardial surface cooling, excessive external myocardial rewarming to 18 degrees to 22 degrees C occurs within 20 minutes at all sites after delivery of the cardioplegic solution.(ABSTRACT TRUNCATED AT 400 WORDS)     

The effectiveness of topical cardiac hypothermia.

The effectiveness of cooling the subendocardial myocardium by five different methods was evaluated in a group of 100 patients. The most effective and consistent method to cool the heart was by total body hypothermia with the heat exchanger in the cardiopulmonary bypass system. Myocardial temperature became equal to vena caval blood temperature after only a one minute lag. The least effective methods of myocardial cooling were those in which a bath of chilled fluid enveloped the outside surface of the heart, with and without aortic cross-clamping. The drop in ventricular septal temperature was so small that topical hypothermia, by itself, may be worthless. Two methods in wich chilled fluid was perfused through the coronary system produced a significant lowering of myocardial temperature. One of these methods employs coronary perfusion with a cold cardioplegic solution in addition to total body hypothermia. It is our current choice for myocardial protection during cross-clamping of the ascending aorta.     

Effect of venting on myocardial protection by hypothermic cardioplegic arrest

Myocardial rewarming between cardioplegic (CP) infusions is in part attributable to blood circulating through the heart from collateral channels. This experiment was performed to determine if the type of left ventricular (LV) venting affects myocardial temperature (temp) or alters myocardial protection. Twelve dogs underwent cardiopulmonary bypass (CPB) at 37 degrees C and were subjected to 100 min of cardioplegic arrest by intermittent coronary infusion of 300 ml 0-4 degrees C CP solution. Arterial, central venous, left atrial, and LV pressures; cardiac output; systemic, septal (S), right ventricular (RV), and LV temp; myocardial ATP and glycogen were measured; LV pressure/volume curves and LV dp/dt were calculated. Group A (6 dogs) had an LV vent during CPB, and Group B (6 dogs) had the aorta vented via the CP line. CP infusion lowered LV temp to 8 degrees C in Group A vs 13 degrees C in Group B (P less than 0.000002); S temp was lowered to 7 degrees C in Group A vs 11 C in Group B (P less than 0.00007); and RV temp was lowered to 16 degrees C in Groups A and B. Ten minutes after CP, LV and S temp increased to 20-21 degrees C in Groups A and B, and RV temp to 24-25 degrees C in Groups A and B. Twenty minutes after CP all temperatures were the same. Hemodynamics and myocardial metabolic studies were similar in the two groups. CONCLUSIONS: Hearts vented via the LV cooled to a lower temperature vs those vented via the aorta. Venting did not affect myocardial rewarming, myocardial metabolites, or ventricular function.     

Optimizing myocardial hypothermia: II. Cooling jacket modifications and clinical results

After induction of myocardial hypothermia by cold cardioplegic solution, myocardial rewarming occurs at 0.5 degrees to 1.0 degrees C/min. In addition to preventing myocardial rewarming from systemic and pulmonary venous return, continuous cooling of the myocardial surface must be provided. Modifications of a previously reported cooling jacket are described. These modifications include decreased width and thickness of the metal skeleton for easier application and increased malleability, respectively. Also, the double-row flow channel markedly minimizes obstruction of flow secondary to kinking and allows inlet and outlet lines to attach at adjacent points of the jacket thus minimizing obstruction of the operative field. The effectiveness of the jacket in 36 patients undergoing valve replacement and 19 patients having pulmonary thromboendarterectomy was evaluated by measurement of myocardial temperatures at multiple sites throughout aortic cross-clamping. Temperatures at all sites were maintained at 12 degrees C or less. Temperatures measured in phrenic nerve pedicles ranged from 25 degrees to 27 degrees C. During cooling, heat removal by the jacket was 330 calories/min. During maintenance of myocardial hypothermia, heat flow was 190 calories/min. Modifications of a cooling jacket facilitate usability and an array of sizes enhances applicability.     

逆行性灌注浅低温氧合血心脏不停跳与冷血心脏停搏液对cTn I的影响

目的　对比研究逆行性灌注浅低温氧合血心脏不停跳与低温冷血心脏停搏液对外周血清心肌肌钙蛋白 I(c Tn I)的影响。　方法　将 18例双瓣膜置换术患者分为心脏不停跳组和心脏停搏组 ,观察围手术期外周血清c Tn I、肌酸激酶 (CK)、肌酸激酶同工酶 (CK- MB)及主动脉阻断前后用透射电子显微镜观察心肌超微结构变化。结果　心脏不停跳组主动脉开放后各个时相点 CK虽略低于心脏停搏组 ,但差别无显著性意义 (P>0 .0 5 ) ;主动脉开放后 6小时 CK- MB明显低于心脏停搏组 (P<0 .0 5 ) ,主动脉开放后各个时相点心脏不停跳组 c Tn I明显低于心脏停搏组 (P<0 .0 5 )。两组患者主动脉阻断前心肌超微结构均有轻度改变 ,主动脉阻断 90分钟心脏停搏组心肌超微结构损伤较心脏不停跳组明显。　结论　逆行性灌注浅低温氧合血心脏不停跳围手术期外周血清 c Tn I较低 ,可能与该方法使体外循环期间发生不可逆损伤的心肌细胞较少 ,心肌超微结构损伤较轻有关。     

Nifedipine as an adjunct to St. Thomas' Hospital cardioplegia. A double-blind, placebo-controlled, randomized clinical trial

The cardioprotective effect of the addition of the slow calcium-channel blocker nifedipine to cardioplegic solution was tested in two double-blind placebo controlled randomized studies. The first study included 24 patients undergoing aortic-coronary bypass grafting, and the second included 24 patients undergoing aortic valve replacement. Nifedipine at a dose of 200 micrograms/L or placebo was added to St. Thomas' Hospital cardioplegic solution. The following markers of ischemia were used: adenosine triphosphate and its catabolites, creatine phosphate and inorganic phosphate, determined in transmural left ventricular biopsy specimens taken before, at the end of, and after aortic cross-clamping; hemodynamic recovery 15 minutes after cessation of cardiopulmonary bypass; clinical outcome in terms of the incidence of arrhythmias, low cardiac output, positive inotropic support immediately after operation, and follow-up at 15 months. The main difference between the two studies was that myocardial temperature during cross-clamping remained constant at 14 degrees C in coronary bypass grafting but increased to 25 degrees C in valve operations despite the application of the same amounts of cardioplegic solutions. This lower temperature resulted in better preservation of high-energy phosphates in coronary bypass operations as compared to the placebo group having valve replacement operations. According to analysis of variance, a drug effect could be demonstrated only in the aortic valve replacement study: Accumulation of breakdown products of the adenine nucleotide pool was less in the nifedipine group than in the placebo group (p less than 0.05). Adenosine triphosphate decreased only to 84% in the nifedipine group and to 72% in the placebo group. Despite this adenosine triphosphate-sparing effect, weaning from cardiopulmonary bypass was more difficult in the nifedipine group. Left ventricular stroke work index 15 minutes after bypass was decreased to 72% of the prebypass value in the nifedipine group (t test, p less than 0.01) and only to 86% in the placebo group (p = NS). In contrast, after the patients were admitted to the intensive care unit, the incidence of low cardiac output tended to be lower in the nifedipine group than in the placebo group: 33% versus 58% (p = NS). In conclusion, ischemia-induced degradation of nucleotides as it occurs when myocardial cooling is inadequate can be prevented by the addition of nifedipine to the St. Thomas' Hospital cardioplegic solution. This effect, however, is not associated with an improved clinical outcome.     

Cold blood cardioplegia.

The technique of myocardial protection by means of a cardioplegic solution consisting of cold blood (10 degrees C) with potassium (30 mEq. per liter) is described. A disposable cooling coil is used and a separate pump head for coronary perfusion is avoided. The aortic perfusion cannula can be used for venting of the left ventricle and subsequently for venting of air. This method was used in 125 consecutive patients undergoing coronary revascularization and in 73 consecutive pediatric cardiac surgical procedures with excellent results.     

Myocardial protection related to magnesium content of cold blood hyperkalemic cardioplegic solutions in CABG

The objective of this study was to investigate whether the addition of magnesium to a hyperkalemic cardioplegic solution containing 1.2-1.5 mmol/L ionized calcium improves myocardial protection. Twenty-seven coronary artery disease (CAD) patients underwent coronary artery bypass grafting (CABG) received hyperkalemic (20-22 mmol/L potassium) cardioplegic solutions containing 1.2-1.5 mmol/L ionized calcium and were randomized to one of the following groups: Group A (n = 9) received 3-4 mmol/L magnesium cool blood cardioplegia (4 degrees C), Group B (n = 9) received 8-10 mmol/L magnesium cold blood cardioplegia (4 degrees C). Group C (n = 9) received 16-18 mmol/L magnesium cold blood cardioplegia (4 degrees C). The effect of myocardium protection of the three kinds of cardioplegic solutions were evaluated by clinical outcome, cTnI and CK-MB mass. Serial venous blood samples were obtained before induction, after cardiopulmonary bypass (CPB), postoperative 6 h, 24 h, 72 h, and 6th day, respectively. The percentage of myocardial autoresusciation in group B (100%) was significantly higher than that in groups A (77.8%) and C (66.7%). One patient in group A and two patients in group C needed an interim pacemaker, but none in group B. The period of postoperative mechanical ventilation and ICU stay in group B was shorter than in the other two groups. The level of cTnI and CK-Mb mass increased from postoperative 6 h (p < .05), reached peak in 24 h-72 h, and recovered postoperative 6th day. As compared with groups A and C, the plasma concentrations of cTnI and CK-MB mass in group B were significantly lower at 6 h, 24 h, and 72 h (p < .01). 8 approximately 10 mmol/L magnesium cold blood cardioplegia provides better myocardium protection than higher or lower concentrations.     

Cardioplegia versus intermittent ischaemic arrest in coronary bypass surgery.

No definitive method of myocardial preservation has been established and conclusions based on experimental data may not be applicable to patients with coronary artery disease. Fifty patients undergoing coronary bypass grafting were randomly assigned to one of two groups for myocardial preservation. In group A cold cardioplegia with external cardiac cooling was used and in group B ischaemic arrest with mild systemic cooling to 32 degrees C. Myocardial preservation was assessed by analysis of enzymes specific to the heart, left ventricular biopsy, and electrocardiography. Equal protection of the myocardium was provided in both groups but the mean cross-clamp time in group A was significantly longer than in group B. This implies that cardioplegia confers greater protection than intermittent ischaemic arrest.     

Myocardial Protection from Permanent Injury during Aortic Cross-Clamping: Effectiveness of Pharmacological Cardiac Arrest Combined with Topical Cardiac Hypothermia

In two groups of animals (6 and 9 dogs), the aorta was cross-clamped 60 and 90 minutes, respectively, during hypothermic cardiopulmonary bypass. Immediately after cross-clamping, pharmacological cardiac arrest was induced by injecting 100 ml of a cold cardioplegic solution into the aortic root. Topical cardiac hypothermia was added. In hearts undergoing 90 minutes of ischemia, a repeat injection of the cardioplegic solution was done at 45 minutes. In 14 dogs (control group), only topical cardiac hypothermia was instituted for myocardial protection during 60 minutes of ischemia. Seven weeks after operation the surviving animals (6 in each group) were killed.Study of myocardial performance failed to demonstrate significant differences among the groups. Microscopic examination of transmural samples taken from anatomically defined sides of both ventricles, disclosed isolated, punctuate subendocardial scars in only 2 hearts of the control group. All the hearts having 90 minutes of pharmacological cardiac arrest and topical cardiac hypothermia exhibited diffuse fibrosis replacing 10 to 20% of the left ventricular myocardium. Extent and incidence of fibrosis were significantly higher in these hearts in comparison to those of the other groups.We conclude that pharmacological cardiac arrest plus topical cardiac hypothermia makes a safe and efficient method of myocardial protection during aortic cross-clamping only if the ischemic interval is limited to 60 minutes. It cannot prevent permanent myocardial injury if the ischemic arrest is extended to 90 minutes.