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.     

Right atrial temperature and electrical activity during cardioplegic cardiac arrest

In 18 patients undergoing coronary artery bypass surgery the relation between right atrial temperature and right atrial electrical reactivation during cardioplegic cardiac arrest was studied. The administration of cardioplegic solution induced immediate ventricular and atrial arrest in all patients. No recurrence of ventricular activity was observed while right atrial activity subsequently recurred in 11 patients. Activity at the surface ECG was recorded only in one patient with right atrial reactivation. No right atrial electrical activity was found below 19 degrees C. The average atrial temperature was 21.5 degrees C while the average apex temperature was 15 degrees C. The study has confirmed previous observations that during cardioplegic cardiac arrest the right atrium is not as well protected as the ventricular tissue against rewarming. Monitoring of the right atrial electrical activity or right atrial temperature is essential to ensure atrial arrest during the entire period of cardioplegic cardiac arrest.     

Cardiomyocyte apoptosis and duration of aortic clamping in pig model of open heart surgery.

OBJECTIVE: Apoptotic cardiomyocyte death is induced during open heart surgery, but its determinants are poorly understood. Prolonged aortic clamping time is associated with adverse clinical outcomes. The purpose of this study was to determine whether occurrence of cardiomyocyte apoptosis is related to the duration of aortic clamping in experimental pig model of cardiac surgery with cardiopulmonary bypass. METHODS: The pigs (mean weight 29 +/- 1 kg) were randomly divided to undergo cardioplegic arrest for 60 (n = 4) or 90 (n = 4) min followed by reperfusion period of 120 min. Control group (n = 5) was connected to cardiopulmonary bypass for 120 min without cardioplegic arrest. Cardiomyocyte apoptosis was detected (TUNEL assay and immunohistochemical staining of active caspase-3) in left ventricular tissue samples obtained before ischemia and after the ischemia-reperfusion period. RESULTS: Apoptotic cardiomyocytes were found in all samples obtained after cardioplegic arrest and cardiopulmonary bypass alone with the TUNEL assay. The amount of apoptosis after the 120 min of cardiopulmonary bypass alone in the control group was 0.006 +/- 0.001%. Compared with this, cardiomyocyte apoptosis was increased after cardioplegic arrest. After 60 min of aortic cross-clamp the amount of apoptosis was 0.019 +/- 0.004% (p = 0.031). After 90 min of aortic cross-clamp the amount was 0.042 +/- 0.005% (p < 0.001) being significantly higher than after 60 min (p = 0.001). Aortic cross-clamp of 90 min also resulted in a detectable increase in caspase-3 activation when compared with controls. CONCLUSIONS: The occurrence of cardiomyocyte apoptosis increases with prolonged aortic clamping time during open heart surgery.     

Atrial activity during cardioplegia and postoperative arrhythmias

Cardioplegia provides excellent protection for the left ventricle, but the right atrium may be poorly protected. Myocardial temperatures, right atrial electrical activity, and postoperative arrhythmias were assessed in 103 patients participating in two consecutive randomized trials comparing blood cardioplegia (n = 36), crystalloid cardioplegia (n = 38), and diltiazem crystalloid cardioplegia (n = 29). Both right atrial and right ventricular temperatures were significantly warmer (p less than 0.05) during delivery of the blood cardioplegic solution than during delivery of either the crystalloid or the diltiazem crystalloid cardioplegic solutions; the aortic root temperatures were 9 degrees +/- 2 degrees C with blood cardioplegia and 5 degrees + 1 degrees C with both crystalloid and diltiazem crystalloid cardioplegia. Atrial activity during cardioplegic arrest was greatest with blood cardioplegia (12 +/- 3 beats/min), lower with crystalloid cardioplegia (10 +/- 2 beats/min), and minimal with diltiazem crystalloid cardioplegia (5 +/- 1 beats/min, p less than 0.05). Perioperative ischemic injury (by creatine kinase MB isoenzyme analysis) was greatest with crystalloid cardioplegia (p less than 0.05). Postoperative supraventricular arrhythmias (both treated and untreated) were more frequent after crystalloid cardioplegia (crystalloid, 63%; blood, 40%; diltiazem, 47%; p less than 0.05). Patients in whom supraventricular arrhythmias developed had significantly more postoperative ischemic injury (by creatinine kinase MB isoenzyme analysis, p less than 0.05). Blood cardioplegia reduced supraventricular arrhythmias by reducing ischemic injury despite warmer intraoperative temperatures and more right atrial activity. Diltiazem crystalloid cardioplegia reduced postoperative arrhythmias by improving intraoperative myocardial protection and suppressing intraoperative and postoperative atrial activity. Crystalloid cardioplegia cooled but did not arrest the right atrium intraoperatively, resulted in the most perioperative ischemic injury, and yielded the highest incidence of postoperative supraventricular arrhythmias.     

Improved myocardial recovery after cardioplegic arrest with an oxygenated crystalloid solution

Possible enhancement of myocardial protection by oxygenation of a crystalloid cardioplegic solution was evaluated in a three-part study. In Part I, canine hearts underwent ischemia followed by heterogeneous cardioplegic arrest for 45 to 60 minutes. Oxygenation led to improved recovery in the left anterior descending region (47% versus 86% recovery, p less than 0.05) (15 minutes of ischemia) and in the circumflex region (9.5% versus 52% recovery, p less than 0.05) (30 minutes of ischemia). Part II was a blind prospective randomized study in 12 patients. It examined creatine kinase, myoglobin, and lactate as well as coronary sinus flow, oxygen consumption, and cardiac work 1 hour after aortic cross-clamping during atrial and during ventricular pacing. No significant difference was demonstrable between control and oxygenated solutions. In Part III, 57 coronary bypass patients were protected with a nonoxygenated solution while 94 patients received an identical oxygenated solution. Twelve-hour creatine kinase levels were similar in the nonoxygenated (9.5 +/- 16 IU, +/- standard deviation) and oxygenated (11 +/- 22 IU) groups if the cross-clamp interval was 28 minutes or less. In patients subjected to longer than 28 minutes of arrest, the 12 hour creatine kinase MB levels were more than twice as high in the nonoxygenated group (26.5 +/- 26 IU) compared to the oxygenated group (9.9 +/- 14 IU, p less than 0.05). In this canine model of heterogeneous cardioplegia and in the routine conduct of coronary bypass operations, oxygenated crystalloid cardioplegia is superior to an identical nonoxygenated solution.     

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.     

Ultrastructural and cytochemical correlates of myocardial protection by cardiac hypothermia in man

We report observations on ultrastructural and cytochemical changes in the myocardium after hypothermic protection in 21 patients who underwent cardiac operation. Two general categories of hypothermic protection were studied. (1) topical cooling during anoxic arrest and moderate general hypothermia (10 patients with aortic valve replacement, Group 1) and (2) intermittent perfusion during moderate general hypothermia combined with topical cooling (11 patients with multiple valve replacement, Group II). Transmural left ventricular biopsies were taken at the start of the cardiopulmonary bypass and shortly after the end of aortic cross-clamping. In Group I (cross-clamp time, 51 +/- 12 minutes) only minor pathologic changes of the myocardial fine structure were found, with no differences among the left ventricular layers. In most mitochondria, structure remained intact but the mitochondrial granules disappeared. Cytochrome-c-oxidase activity was unchanged. In Group II (total cross-clamp time, 83 +/- 16 minutes) the subendocardium was well preserved. Slight subcellular damage comparable with that of resulting from topical cooling was seen in all hearts even after a total cross-clamp period of 106 minutes. Cytochrome-c-oxidase activity was unchanged. In the subepicardium, however, a positive correlation was found between the severity of ultrastructural damage and total cross-clamp time (p less than 0.05). Matrix clearing, damage to the cristae and the mitochondrial membranes, and nuclear abnormalities occurred when the aorta was cross-clamped for morethan 60 minutes. Cytochrome-c-oxidase activities decreased in these samples. It is concluded that: (1) no significant subcellular injury was found in hearts cooled topically during 1 hour of anoxic arrest; and (2) in hearts protected by intermittent perfusion during moderate general hypothermia and additional external cooling, the subendocardium was well preserved for anoxic periods of up to 106 minutes. However, after 60 minutes of aortic cross-clamping subcellular damage increased progressively in the subepicardium.     

The effect of augmented atrial hypothermia on atrial refractory period, conduction, and atrial flutter/fibrillation in the canine heart.

The purpose of this study was to test the assumption that the cause for postoperative atrial flutter/fibrillation after cardiopulmonary bypass is inadequate atrial myocardial protection. Dogs were subjected to cardioplegic arrest for 60 minutes without augmented atrial hypothermia (seven dogs, control group) or augmented atrial hypothermia with topical atrial cooling (seven dogs, study group). Twenty-five electrodes (15 on the right atrium and 10 on the left atrium) were fixed on the atria to measure effective refractory period and conduction time. Data were taken before bypass, immediately after bypass, and 2 hours after bypass. During cardioplegic arrest the mean temperatures measured in the atria were significantly lower (p less than 0.001) in the study group (13.5 degrees +/- 7.0 degrees C) than in the control group (23.7 degrees +/- 3.2 degrees C). There was no significant change in the mean effective refractory period after bypass in the control or study groups or in the prevalence of inducibility of atrial flutter/fibrillation by extrastimulation (3/7 dogs in the control group and 2/7 in the study group). During right atrial pacing, total conduction times were significantly longer (p less than 0.025 at cycle lengths of 300 and 350 msec) in the control group (74 +/- 5 msec and 75 +/- 7 msec, respectively) than in the study group (65 +/- 9 msec and 64 +/- 8 msec, respectively) immediately after bypass. Two hours after bypass, however, there were no significant differences under the same conditions between the two groups. There were no significant differences in conduction during left atrial pacing after bypass. Comparing those atria that were inducible with those not inducible demonstrated a significantly increased dispersion of effective refractory period (90 +/- 23 msec versus 74 +/- 18 msec, p less than 0.05) and increased conduction time in the inducible group. We concluded that augmented atrial hypothermia during cardioplegic arrest had no effect on the inducibility of fibrillation, had no effect on repolarization, and had only a small effect on conduction, which resolved within 2 hours after bypass. However, the study demonstrates that when the atria are inducible the substrates are an increased dispersion of refractoriness and a prolongation of conduction time.     

Tachyarrhythmias and triggering factors for atrial fibrillation after coronary artery bypass operations

BACKGROUND: We evaluated the role of supraventricular arrhythmias and assessed clinical predictors of atrial fibrillation (AF) that developed after coronary artery bypass operations. METHODS: Eighty patients, with a mean age of 65.8 years, underwent 24-hour Holter monitoring preoperatively and for 4 consecutive days postoperatively, or until clinically documented AF, for analysis of the number of premature beats and tachyarrhythmias. Atrial areas and atrial peptides were measured preoperatively and postoperatively. RESULTS: Twenty-nine of 80 (36.3%) patients had postoperative AF. Preoperatively, the maximal supraventricular premature beats per minute were higher in the AF group (p = 0.02). The body mass index and total amount of cardioplegia were lower (p = 0.02 and p = 0.006, respectively), and withdrawal of beta-blockers postoperatively more frequent (p = 0.001) in the AF group, but atrial areas and atrial peptides did not differ. CONCLUSIONS: Frequent supraventricular premature beats preoperatively may indicate a propensity for AF. A larger amount of cardioplegia during the cross-clamp period may reduce the risk of postoperative AF. Further studies are mandatory to clarify why patients with lower body mass index were more prone to AF.     

Decreased incidence of supraventricular arrhythmias achieved by selective atrial cooling during aortic valve replacement

Inadequate atrial hypothermia and subsequent ischemic injury have been recognized as the major causes of supraventricular arrhythmias (SVAs) and conduction defects following cold chemical cardioplegia. This study was designed to assess the effects of right atrial cooling (15 degrees-20 degrees C) during cardioplegic arrest upon the incidence of postoperative SVAs and conduction defects in 40 consecutive patients undergoing isolated aortic valve replacement. Atrial preservation was ensured by combining systemic (24 degrees C) and topical hypothermia with snared double caval cannulation during arrest. Myocardial temperatures in the right atrial septum and anterior wall of the right ventricle were recorded before and after each cardioplegic infusion and upon release of caval tapes. Postoperatively, the incidence of SVAs and conduction defects was assessed by continuous rhythm monitoring, bipolar atrial electrograms and, in ten patients, 24-h Holter recordings during the first postoperative day. With the venae cavae snared, temperatures in the right atrial septum were not significantly different from those measured simultaneously in the right ventricle. Release of caval tapes resulted in right atrial temperatures increasing to systemic temperature (from 17.1 +/- 2.9 degrees C to 25.9 +/- 5.6 degrees C [m +/- SD]; P less than 0.01). Atrial rewarming between cardioplegic infusions did not exceed 2.9 degrees +/- 3.2 degrees C. Postoperatively, four patients (10%) developed sustained atrial fibrillation. One additional patient had a single episode of paroxysmal atrial fibrillation and two patients experienced asymptomatic episodes of junctional rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of cardioplegic arrest on right atrial function

Atrial electrical and mechanical activity persists during cardioplegic arrest. It has been postulated that atrial ischemia may occur and cause deterioration in atrial function. This study was designed to assess the effect of cardioplegic arrest on right atrial function. Twenty-one pigs were placed on cardiopulmonary bypass (CPB), and the right atrium was isolated from the circulation by snaring both venae cavae and incising the coronary sinus. The tricuspid valve was closed through a small right ventriculotomy, and baseline atrial function was assessed using a compliant balloon in the atrium. Fourteen pigs underwent one hour of cardioplegic arrest (7 with cardioplegia alone [CCA group] and 7 with the addition of topical hypothermia [CCA + TH group]) followed by one hour of normothermic reperfusion. Seven other pigs were placed on CPB for the same period of time (CPB group). Atrial electrical and mechanical activity persisted at 45 beats per minute in the CCA group but was virtually abolished in the CCA + TH group. Cardioplegic arrest caused considerable deterioration in right atrial function (developed pressure, 18.9 +/- 0.8 [baseline] versus 14.1 +/- 0.7 mm Hg; p less than 0.05; first derivative of atrial pressure [dP/dt], 187 +/- 19 versus 134 +/- 25 mm Hg per second; p less than 0.05; 60 minutes of reperfusion and balloon volume of 20 ml). It was not affected by topical cooling. Right atrial developed pressure was maintained, but dP/dt was significantly reduced in the CPB group. This study suggests that cardioplegic arrest does not protect the atrium.     

Ultrastructural myocardial preservation during coronary artery surgery: a controlled, prospective, randomized study in humans

Potassium cardioplegia was compared with normothermic, intermittent ischemic arrest in 30 patients undergoing multiple coronary artery bypass grafts. Group 1 comprised 15 patients in whom cold potassium cardioplegia with St. Thomas' Hospital solution was used. In Group 2 were 15 patients who underwent intermittent ischemic arrest during the construction of the distal anastomoses. Two myocardial transmural left ventricular biopsies were done in each patient. There was no operative mortality. Electron microscopical examination showed normal myocardial ultrastructure in both groups. In particular, mitochondria were well preserved in all samples. The postoperative electrocardiogram demonstrated a new Q wave in 1 patient in Group 2 whose level of the myocardial isoenzyme of creatine phosphokinase (CPK-MB) was within the normal range. The peak CPK-MB release in Group 1 was 23.2 +/- 20.1 IU and in Group 2, 19.9 +/- 15.1 IU. This difference was not statistically significant. The mean period of anoxic arrest in Group 1 was 49.5 +/- 15 minutes and in Group 2, 25.5 +/- 8 minutes (p less than 0.001). Total cardiopulmonary bypass time in Group 1 was 114.5 +/- 20 minutes and in Group 2, 90.2 +/- 16 minutes (p less than 0.01). It is concluded that both techniques can preserve myocardial subcellular architecture during multiple coronary artery bypass grafting in patients with normal left ventricular function.     

Cold cardioplegia versus hypothermia for myocardial protection. Randomized clinical study.

Seventeen of 34 consecutive patients undergoing coronary artery bypass grafting were randomly assigned to one of two methods of myocardial preservation. With the cold cardioplegic method (Group A), a 4 degrees C. asanguineous solution with 30 mEq. of potassium per liter was infused into the aortic root for about 2 minutes immediately after aortic cross-clamping and again after about 45 minutes or when myocardial temperature rose above 19 degrees C. External cardiac cooling was provided by constant infusion of 4 degrees C. Ringer's solution into the pericardium. Seventeen patients were assigned to simple cardiac cooling by hypothermic systemic perfusion before aortic cross-clamping plus external cardiac cooling (Group B). Electromechanical activity ceased within 1 to 2 minutes in Group A but continued throughout the ischemic period in 14 patients in Group B. Myocardial temperature (mean for all observations) during aortic cross-clamping was 17.2 +/- 0.44 degrees C. In Group A and 24.0 +/- 0.70 degrees C. in Group B. Operating conditions were better in Group A. Card-ac function early postoperatively was good in both groups clinically and according to measurements, but only in the cold cardioplegic group (A) was cardiac index not adversely affected by longer cross-clamp time. Myocardial necrosis occurred in both groups but was probably less in the cold cardioplegic group. Thirteen patients (76 percent) in Group A had no electrocardiographic evidence of myocardial injury, compared with eight (47 percent) in Group B (p = 0.08). Eleven (65 percent of Group A had no or short-lived appearance of ceatine phosphokinase isoenzyme (CK-MB), compared with six (35 percent) of Group B (p = 0.08). Time-related CK-MB and SGOT mean levels were consistently lower in Group A.     

Simultaneous antegrade and retrograde reperfusion after cardioplegic arrest for coronary artery bypass

Retrograde coronary sinus reperfusion with warm blood during proximal anastomoses permits completion of myocardial revascularization under a single cross-clamp application. Reperfusion with both antegrade (via arterial and vein grafts) and retrograde (via coronary sinus catheter) warm blood has raised concerns about maldistribution of perfusate or overpressurization of capillary beds. This prospective, randomized design compares postcardioplegic myocardial recovery among patients receiving retrograde reperfusion only and patients receiving simultaneous antegrade/retrograde reperfusion. Twenty-four patients were selected among all presenting as outpatients for elective coronary artery bypass (CAB). Each patient underwent CAB with cardioplegic arrest and single cross-clamp technique. During proximal anastomoses the heart was reperfused with warm blood from the cardiopulmonary bypass (CPB) circuit. Twelve received retrograde reperfusion only, and 12 received simultaneous antegrade/retrograde reperfusion via an internal mammary artery (IMA) graft, all vein grafts, and the coronary sinus catheter. Vein graft perfusion was interrupted in each vein as the proximal anastomosis was performed. Myocardial recovery time (interval from initiating reperfusion until electrical and mechanical activity), cardioversion incidence, requirement for inotropic support, and Swan-Ganz hemodynamic parameters measured immediately 6 and 24 hours postoperatively were compared between groups. There were no differences between groups in age, ventricular function, number of grafts, or CPB time. Also, there were no differences in cardioversion, inotropic need, or postoperative hemodynamic performance. Myocardial recovery time was reduced in patients receiving simultaneous antegrade/retrograde reperfusion (13.9+/-7.0 vs 2.6+/-2.1 minutes). Simultaneous reperfusion of warm blood antegrade and retrograde is not deleterious to the myocardium. More rapid recovery of myocardial function may represent a shorter period of warm ischemia but does not appear to translate to improved postoperative myocardial performance.     

Cardioplegic arrest does not increase the risk of atrial fibrillation after coronary artery bypass surgery.

OBJECTIVE: Atrial fibrillation (AF) is the most common arrhythmia after coronary artery bypass grafting (CABG). It is a considerable source of morbidity, prolongs hospital stay and increases costs of treatment. Atrial cannulation, cardiopulmonary bypass and cardioplegic arrest have been suggested to play a role in the development of AF after CABG. The aim of this case-control study was to evaluate the role of cardiopulmonary bypass and cardioplegic arrest in the development of postoperative AF. METHODS: Data from 114 patients undergoing CABG without cardiopulmonary bypass and cardioplegic arrest (off-pump) between October, 1998 and December, 2002 were evaluated for the occurrence of postoperative AF. Each patient was individually matched by gender, age (+/-3 years), left ventricle ejection fraction (+/-5%), history of myocardial infarction, unstable angina, and beta-blocker medication with patients undergoing CABG with cardiopulmonary bypass and cardioplegic arrest (on-pump) during the same period. The data from off-pump and on-pump groups were compared. RESULTS: Off-pump and on-pump groups had similar preoperative characteristics. The number of distal anastomoses was lower in the off-pump (2.3+/-0.9) than in the on-pump (3.9+/-1.1, (P<0.001) group. However, the incidence of postoperative AF in the off-pump (36.8%) and the on-pump groups (36.0%) did not differ from each other. Old age was the only independent predictor of AF after CABG. CONCLUSIONS: Neither cardiopulmonary bypass nor cardioplegic arrest increases the risk of postoperative AF after CABG.     

Comparison of blood cardioplegia to electrolyte cardioplegia on the effectiveness of preservation of right atrial myocardium: mitochondrial morphometric study

The right atrium differs from the left ventricle in two respects during cardioplegic arrest: a higher proportion of noncoronary collateral flow is delivered to the right atrium, and the atrium is frequently excluded from topical ice cooling because of its higher position relative to the left ventricle. These factors result in early rewarming of atrial myocardium. To the best of our knowledge, the surgical literature contains no reports on whether blood cardioplegia can provide better atrial myocardial preservation than electrolyte cardioplegia. Twenty consecutive patients who underwent cardiac operations were randomly selected to receive blood cardioplegia (Group 1) or electrolyte cardioplegia (Group 2). Hypothermia was achieved by systemic cooling and continuous topical cooling with ice slush. Stereological morphometric study of mitochondria was performed on 40 biopsy specimens taken from the right atrium prior to aortic cross-clamping (preischemia) and at the end of ischemia. In Group 1, total aortic cross-clamp time was 72.8 +/- 32.5 minutes. The mean mitochondrial surface area before ischemia was 0.224 +/- 0.032 mu 2 and after ischemia, 0.336 +/- 0.032 mu 2, a 50.0% increase in mitochondrial size. In Group 2, total aortic cross-clamp time was 69.7 +/- 30.9 minutes. The mean mitochondrial surface area before ischemia was 0.205 +/- 0.025 mu 2 and after ischemia, 0.439 +/- 0.111 mu 2, an average increase in mitochondrial size of 114.2%. There was no significant difference between the two groups in mitochondrial size before ischemia. However, after ischemia the mean mitochondrial surface areas were significantly different (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Temporal endothelin dynamics of the myocardial interstitium and systemic circulation in cardiopulmonary bypass

OBJECTIVE: Increased systemic levels of the bioactive peptide endothelin 1 during and after cardioplegic arrest and cardiopulmonary bypass have been well documented. However, endothelin 1 is synthesized locally, and therefore myocardial endothelin 1 production during and after cardiopulmonary bypass remains unknown. METHODS: Pigs (n = 11) were instrumented for cardiopulmonary bypass, and cardioplegic arrest was initiated. Myocardial interstitial and systemic arterial levels of endothelin 1 were measured before cardiopulmonary bypass, throughout bypass and cardioplegic arrest (90 minutes), and up to 90 minutes after separation from bypass. Myocardial interstitial endothelin 1 was determined by microdialysis and radioimmunoassay. RESULTS: Baseline myocardial endothelin 1 levels were higher than systemic endothelin 1 levels (25.6 +/- 6.7 vs 8.3 +/- 1.1 fmol/mL, P <.05). With the onset of bypass, myocardial endothelin 1 increased by 327% +/- 92% from baseline (P <.05), which preceded the increase in systemic endothelin 1 levels. CONCLUSION: Myocardial compartmentalization of endothelin 1 exists in vivo. Cardiopulmonary bypass and cardioplegic arrest induce temporal differences in endothelin 1 levels within the myocardial interstitium and systemic circulation, which, in turn, may influence left ventricular function in the postbypass period.     

Electrophysiological evaluation of retrograde cardioplegia--experimental study of efficacy for the right ventricle

Recently, coronary artery bypass grafting operations for patients with total proximal multi-vessel coronary obstructions are increased. In these cases, antegrade cardioplegia through the aortic root has been applied as usual. But it seems to be difficult to deliver cardioplegic solution to myocardium uniformly beyond coronary stenosis. Retrograde coronary sinus cardioplegia in the presence of proximal coronary artery obstruction could maintain improved cardioplegic delivery and satisfactory myocardial protection. Because of the limitation of antegrade cardioplegia, retrograde cardioplegic technique has, once again, been cited as a reasonable alternative to antegrade cardioplegia. But on the other hand, retrograde cardioplegia includes the potential for relatively inadequate preservation of right ventricle based on the venous drainage communication to the coronary sinus. The object of the present work is mainly to evaluate the efficacy of retrograde coronary sinus cardioplegic technique for right ventricle by electrophysiological method. Thirty-six adult mongrel dogs divided three groups. Sixteen animals (Group I) received GIK cardioplegia through the coronary sinus, thirteen animals (Group II) received GIK added diltiazem cardioplegia through the same way, and seven animals (Group III) received GIK cardioplegia through aortic root. No large temperature gradients of myocardium between right and left ventricle in each group and also temperature gradients of right ventricle between three groups have been observed. The time duration from starting of injection of cardioplegia to disappear the electrical activity in right and left ventricle were 11.4 +/- 8.2, 3.4 +/- 1.2 minutes in group I, 2.9 +/- 1.5, 2.2 +/- 1.4 minutes in group II, and 0.9 +/- 0.4, 0.9 +/- 0.2 minutes in group III. The time duration from starting of injection of cardioplegia to reappear the electrical activity in right and left ventricle were 6.4 +/- 8.7, 13.4 +/- 7.9 minutes in group I, 20.0 +/- 3.5, 21.3 +/- 1.6 minutes in group II and 18.0 +/- 5.5, 18.7 +/- 4.5 minutes in group III. Unipolar peak-to-peak amplitude (UPPA) analysis reveals the condition of myocardial preservation during ischemic arrest and we compared preischemic UPPA with post-ischemic UPPA. In group I, UPPA declined of 44.1 +/- 29.3% in right ventricle and 72.7 +/- 27.6% in left ventricle, in group II, 78.7 +/- 28.7%, 81.9 +/- 23.6%, in group III, 71.4 +/- 18.7%, 76.7 +/- 9.89%. Analysis of ultrastructural changes in the myocardium are shown that injury was most manifest in the right ventricle of group I, but in group II, ultrastructure of right ventricle maintained nearly normal condition.(ABSTRACT TRUNCATED AT 400 WORDS)     

Is adenosine preconditioning truly cardioprotective in coronary artery bypass surgery?

BACKGROUND: The large number of experimental studies showing that adenosine "turns on" the protein kinase C (PKC)-mediated pathway that accounts for the cardioprotection conferred by ischemic preconditioning contrasts with the scarcity of clinical data documenting the preconditioning-like protective effect of adenosine during cardiac operations on humans. METHODS: Forty-five patients undergoing coronary artery bypass were randomized to receive, after the onset of cardiopulmonary bypass, a 5-minute infusion of adenosine (140 microg x kg(-1) x min(-1)) followed by 10 minutes of washout before cardioplegic arrest (n = 23) or an equivalent period (15 minutes) of prearrest drug-free bypass (controls, n = 22). Outcome measurements included troponin I release over the first 48 postoperative hours and activity of ecto-5'-nucleotidase, an admitted reporter of PKC activation, as assessed on right atrial biopsies taken before bypass and at the end of the preconditioning protocol (or after 15 minutes of bypass in control patients). RESULTS: Aortic cross-clamping times were not different between the two groups. Likewise, prebypass values of ecto-5'-nucleotidase (nanomoles/mg protein per minute) were similar in control (3.14+/-1.02) and adenosine-treated (2.66+/-1.08) patients. They subsequently remained unchanged in control patients (3.87+/-1.65) whereas they significantly increased after adenosine preconditioning (4.47+/-1.96, p<0.001 versus base line values). However, peak postoperative values of troponin I (microg/L) were not significantly different between control (4.8+/-2.8) and adenosine-preconditioned patients (5.9+/-6.6) nor were the areas under the curve. There were no adverse effects related to adenosine. CONCLUSIONS: Adenosine, given at a clinically safe dose, can turn on the PKC-mediated signaling pathway involved in preconditioning but this biochemical event does not translate into reduced cell necrosis after coronary artery surgery, suggesting that a preconditioning-like protocol may not be the best suited for exploiting the otherwise well-documented cardioprotective effetcs of adenosine.     

Myocardial Antioxidant Defenses During Cardiopulmonary Bypass

A bstract In 31 male patients undergoing coronary bypass surgery who underwent different periods of cardioplegic hypothermic arrest, the activities of glutathione peroxidase, glutathione reductase, glutathione transferase, copper/zinc-containing and manganese-containing super-oxide dismutases, and catalase were studied in the right atrial myocardium, before and 5 minutes after aortic cross-clamping. The levels of thiobarbituric acid reactive substances (TBARS) and nonproteic thiol compounds (NP-SH) were also assessed. Prolonged ischemia followed by reperfusion induced activation of the major myocardial antioxidant enzymes with marked NP-SH depression and TBARS increase, despite cold crystalloid cardioplegic protection. These changes were significantly related to the duration of the ischemic arrest, suggesting: (1) that reperfusion free radical generation is dependent on the severity of the previous ischemic period; and (2) the occurrence of myocardial oxidative stress during cardiopulmonary bypass.