摘要:

Background The purpose of the present study was to evaluate the effects of the maze procedure on atrial function in patients operated on for atrial fibrillation.The maze procedure is a new surgical intervention that is designed to restore sinus rhythm and active mechanical atrial contraction as a definitive treatment for patients with atrial fibrillation.Methods and Results Doppler echocardiographic analysis of mitral and tricuspid inflow as well as pulmonary venous flow velocity was carried out in 46 patients 8+-7 months after the maze procedure, and results were compared with those obtained from 27 age-matched control subjects. To evaluate atrial contraction, we determined the presence of atrial contribution to ventricular filling at the mitral and tricuspid valve levels and measured the percent atrial filling fractions of the left and right atria. To evaluate atrial compliance, we measured the systolic and the systolic-to-diastolic flow velocity ratios of the pulmonary venous inflow. Results were compared with similar measurements obtained from control subjects. Restoration of active atrial contraction was detected in 40 of the 46 patients (87%); right atrial contraction was noted in 38 patients (83%), and left atrial contraction was noted in 28 patients (61%). In patients with active atrial contraction, the percent atrial filling fraction of the right atrium was comparable to that of control subjects (32+-7% versus 33+-8%, P=NS), whereas that of the left atrium was smaller (20+-5% versus 36+-7%, P<.005). In addition, compared with control subjects, pulmonary venous flow in maze patients exhibited a reduced systolic component (17+-4 versus 53+-16 cm/s, P<.001) and decreased systolic-to-diastolic flow velocity ratio (0.3+-0.01 versus 1.1+-0.3, P<.001) and velocity integral ratio (0.3+-0.01 versus 1.3+-0.4, P<.001), all suggesting decreased left atrial filling.Conclusions The maze procedure restores active right atrial contraction and improves left atrial contraction in most patients.Obtained measurements suggest decreased left atrial compliance and reduced left atrial contribution to ventricular filling compared with control subjects. Despite the reduced indexes, qualitative restoration of function in either atria should translate in improved atrioventricular synchrony and reduction in thromboembolic events in patients with chronic or paroxysmal atrial fibrillation. (Circulation. 1994;90(part 2):II-285-II-292.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Reperfusion arrhythmias that follow regional ischemia at normothermia have been studied extensively and are considered to be a manifestation of ischemia-reperfusion injury. In contrast, reperfusion arrhythmias that occur following hypothermic cardioplegic arrest have received little attention from investigators. This study defines the electrophysiological mechanisms for postcardioplegia reperfusion ventricular fibrillation (RVF).Methods and Results The electrophysiology of postcardioplegia RVF was examined by using in situ porcine hearts.Complete heart block was created by using cryoablation before cardioplegic arrest so that isolated ventricular electrical activity could be observed for a prolonged time after reperfusion. Electrophysiological data were collected from limb leads, right atrial electrodes, and left ventricular electrodes in all 12 pigs. In 5 pigs, right and left ventricular endocardial electrograms were also recorded. A total of 103 episodes of RVF were analyzed. In 90 instances, an accelerating automatic ventricular focus initiated RVF. In five animals, RVF occurred after ventricular pacing (ie, purely re-entrant RVF). The mechanism for RVF was indeterminant in 8 instances. The origin of RVF was mapped in 44 instances. RVF usually originated in the left ventricle (25 instances) or septum (16 instances).Conclusions Enhanced automaticity and re-entry are the mechanisms for postcardioplegia and regional ischemia-reperfusion arrhythmias. This finding supports the use of postcardioplegia RVF as a variable for comparing strategies for myocardial protection and suggests that information generated by the study of regional ischemia reperfusion arrhythmias can be used to understand postcardioplegia reperfusion arrhythmias and ischemia-reperfusion injury. (Circulation. 1994;90 (part 2):II-293-II-298.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Both heat-shock protein (HSP) 70 and its mRNA are induced in the ischemic myocardium. The inductor stimuli are, however, not known. Stretch and ischemic metabolic alterations are the two most likely HSP70 inductors.Methods and Results To assess whether anaerobic metabolism induces HSP70 mRNA expression, 61 rat hearts were perfused with Krebs-Henseleit buffer (37 degrees C) in a modified Langendorff apparatus built for rapid switching between pressure-controlled and flow-controlled perfusions. Each heart was initially perfused for 30 minutes at a constant perfusion pressure of 65 mm Hg. Subsequently, separate hearts were perfused at a constant flow of 8, 6, 4, 2, 1, 0.5, or 0 mL/min for 30 minutes using a nonpulsatile pump (n=5, each perfusion level). Hemodynamic measurements demonstrated a linear correlation between coronary flow and both perfusion pressure and developed pressure (r=.94 and r=.89, respectively; P<.0001 for both comparisons). Diastolic pressure at the end of the perfusions increased only in globally ischemic hearts (34+-3 mm Hg at 0 mL/min versus 5+-1 mm Hg at 8 mL/min; mean+-SEM, P<.05). The highest lactate release during the 30-minute constant-flow period was observed at a flow level of 4 mL/min (177+-1 versus 71+-8 micromole at 8 mL/min). Creatine kinase release was detected at 2 mL/min (28+-8 mU/mL after 25 minutes of constant flow versus <8 mU/mL at 4 mL/min). The highest flow level showing cessation of mechanical activity despite pacing of the hearts was at 2 mL/min (2 of 5 hearts). An increased level of HSP70 mRNA expression was found only at 4 mL/min (10-fold increase). Blocking lactate production by substituting glucose with 2-deoxyglucose in the perfusion buffer reduced the HSP70 mRNA level by 44% at 4 mL/min. No increase of HSP70 was detected (Western blots) at any flow level.Conclusions These results indicate that anaerobic metabolism is a strong stimulus for HSP70 transcription and that cessation of anaerobic metabolism in severe ischemia is associated with a shutdown of HSP70 mRNA expression.(Circulation. 1994;90(part 2):II-299-II-305.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Although retrograde warm continuous cardioplegia (RWCC) has been recently advocated as a method of myocardial preservation during cardiac surgery, scant data exist on the effects of RWCC on right ventricular function.However, previous data have clearly shown that retrograde cardioplegia is poorly distributed to the right ventricle and interventricular septum. This experiment was performed to analyze functional preservation of the right ventricle after RWCC.Methods and Results Fourteen mongrel dogs were instrumented with sonomicrometers and pressure transducers to determine left and right ventricular (LV, RV) pressure-volume relationships and placed on cardiopulmonary bypass. All dogs underwent 90 minutes of aortic cross-clamping with either (1) RWCC (n=7) after antegrade warm arrest or (2) retrograde cold multidose cardioplegia (RCMC) (n=7) with topical hypothermia after antegrade cold arrest. All dogs received identical blood cardioplegia solutions. Ventricular function was measured before arrest and 30 and 60 minutes after unclamping. The end-diastolic-work area relationship was calculated, and the slope is presented as percent of baseline (mean+-SEM; repeated measures ANOVA). At 30 minutes after unclamping, RWCC provided 68.77+-9.09 for the left ventricle and 41.03+-7.49 (P<.05 for RWCC versus RCMC for RV function at 30 minutes) for the right ventricle, and RCMC provided 62.80+-7.23 for the left ventricle and 79.40+-13.82 for the right ventricle. At 60 minutes after unclamping, RWCC provided 58.24+-12.35 for the left ventricle and 48.05+-9.72 for the right ventricle, and RCMC provided 65.38+-6.76 for the left ventricle and 61.95+-8.70 for the right ventricle. (P=NS for RWCC versus RCMC for LV function at either 30 or 60 minutes.) These results demonstrate depressed recovery of RV function after 90 minutes of RWCC (P<.05 at 30 minutes after reperfusion) compared with RCMC. No difference in recovery of LV function was detected.Conclusion RWCC may be harmful to the right ventricle and should be used with caution, particularly in patients with preexisting RV hypertrophy.(Circulation. 1994;90(part 2): II-306-II-309.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Retrograde warm blood cardioplegia is now recognized as an effective method of myocardial protection, but concerns persist about its ability to adequately preserve the right ventricle.Methods and Results A total of 75 patients in whom warm blood cardioplegia was continuously given through the coronary sinus were included in this three-part study. Part 1, which involved 30 patients undergoing coronary artery bypass grafting operations, was designed to assess whether the right ventricle incurred a greater degree of anaerobic metabolism than the left ventricle during warm arrest. Immediately before aortic unclamping, antegrade perfusion was resumed and, within 1 minute of washout, blood samples were simultaneously taken from the right ventricle and coronary sinus and assayed for lactate. There was no significant difference in lactate concentrations between the two sampling sites (right ventricle, 2.53+-0.1 mmol/L; coronary sinus, 2.47+-0.1 mmol/L). Part 2 focused on recovery of function. A complete set of postoperative hemodynamic measurements was obtained in 15 among the 30 patients enrolled in part 1 and compared with that obtained in 15 case-matched patients who received conventional cold antegrade crystalloid cardioplegia. Postoperative right ventricular stroke work index was not significantly different between the two groups (retrograde warm, 4.6+-0.2 g m-1m-2; antegrade cold, 4.8+-0.2 g m-1m-2). Part 3 was also targeted at functional end points but in 30 additional patients undergoing reoperative mitral valve replacement and consequently deemed to be at higher risk of right ventricular ischemia. Fifteen patients who received retrograde warm cardioplegia were compared with 15 case-matched control subjects in whom antegrade cold crystalloid cardioplegia was used. In keeping with data of part 3, postoperative right ventricular stroke work index was not significantly different between the two groups (retrograde warm, 6.9+-0.4 g m-1m-2; antegrade cold, 7.7+-0.5 g m-1m-2), nor was there a difference in clinical outcomes or biological recoveries of hepatic function.Conclusions Inadequate protection of the right ventricle associated with the use of retrograde warm blood cardioplegia does not appear to be a clinically founded concern since this technique preserves right ventricular function to the same extent as conventional antegrade cold cardioplegia does.(Circulation. 1994;90(part 2):II-310-II-315.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion.We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ((Ca2+)i) level in isolated rat hearts.Methods and Results Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The (Ca2+)iwas monitored by loading the heart with fura-2 acetoxymethyl ester and by using a (Ca2+)ianalyzer. (Ca2+)iwas calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n=6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+(15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of (Ca2+)iwere comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, (Ca2+)iincreased significantly during reperfusion (from 221+-24 nmol/L (mean+-SEM) at baseline to 341+-19 at the end of reperfusion, P<.05). CPS perfusion at 20 degrees C also induced significant Ca2+overloading during reperfusion, but not as much as in the 4 degrees C group. No significant (Ca2+)iincrease occurred at 28 degrees C or 37 degrees C.Conclusions Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+accumulation.These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia. (Circulation. 1994;90(part 2):II-316-II-320.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background There is continued controversy over the management of pH during ischemia and reperfusion.Calcium overload is an integral feature of the injury resulting from ischemia and reperfusion, and hydrogen ions are known to blunt Ca2+influx into cells because H+inhibits the Na (+) -Ca2+exchange and the slow calcium channels. Hypercarbia is one source of H+, but elevated CO2level is also known to be a potent coronary vasodilator, which may be beneficial during early reperfusion. This study was designed to explore the effect of respiratory and metabolic acidosis during the initial phases of reperfusion after hypothermic cardioplegic ischemia in the neonatal lamb.Methods and Results Forty isolated, blood-perfused neonatal lamb hearts underwent 2 hours of cold cardioplegic ischemia followed by reperfusion with blood with various pH values. pH was controlled either by altering the Fico (2) in the ventilating gas to the oxygenator (groups A through D) or by adding HCl to the reperfusate (group E). pH of the initial reperfusate was 6.8 in group A, 7.1 in group B, 7.5 in group C, and 7.8 in group D. In these groups, pH values were maintained for the initial 5 minutes of reperfusion and then corrected to 7.4 over 20 minutes by changing the Fico2to the oxygenator. In group E, HCl was added to the reperfusate to give pH 6.8 (metabolic acidosis). pH was corrected after 5 minutes of reperfusion by administration of NaHCO3and THAM over the next 15 minutes. At 30 and 60 minutes of reperfusion, left ventricular maximum developed pressure, dP/dt, -dP/dt, maximum developed pressure at V10(volume that gave left ventricular end-diastolic pressure of 10 mm Hg during baseline measurements), and dP/dt at V10were measured. Coronary blood flow and oxygen consumption (MVo2) were also measured to evaluate the metabolic recovery. Group A showed better functional recovery than groups B, C, or D (maximum dP/dt V10: group A, 88.3+-7.7%; group B, 69.3+-10.8%; group C, 74.6+-10.3%; group D, 66.1+-9.4%; and group E, 73.7+-13.8% at 30 minutes (P<.05); group A, 76.1+-13.6%; group B, 61.9+-8.6%; group C, 63.8+-5.4%; group D, 57.9+-9.4%; and group E, 62.6+-12.7% at 60 minutes (P<.05)). Coronary blood flow was higher in group A than in other groups (A, 177.2+-29.6%; B, 144.1+-18.1%; C, 127.3+-18.5%; D, 150.4+-24.3%; and E, 106.0+-20.0% (P<.05)). There were no significant differences in MVo2.Conclusions These data indicate that hypercarbic reperfusion (pH 6.8) for a short period after ischemia improved functional recovery after cold cardioplegic ischemia in neonatal lamb hearts but that metabolic acidosis to an equivalent pH did not improve postischemic function. Possible mechanisms for this effect include reduction of calcium loading to the myocardium through H+inhibition of calcium uptake or the induction of coronary vasodilation by hypercarbia. (Circulation. 1994;90(part 2):II-321-II-327.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Standard myocardial protection during cardiac surgery uses hypothermic arrest, but warm heart surgery, recently introduced, is now used in many centers.We hypothesized that warm continuous blood cardioplegia (WCBC) would provide better myocardial preservation than cold continuous blood cardioplegia (CCBC).Methods and Results In isolated cross-perfused canine hearts, left ventricular (LV) function and myocardial O2consumption (MVo2) were measured at constant LV volume, coronary perfusion pressure, and heart rate before and after 75 minutes of arrest at 37 degrees C or 10 degrees C. Metabolism was evaluated by Phosphorus-31 nuclear magnetic resonance spectroscopy. LV resting tone increased transiently after arrest by CCBC but not WCBC (38+-3.9 versus 2.9+-0.5 mm Hg, P<.0005). Myocardial ATP changed over time differently in the groups (P<.001), declining at the outset of CCBC and returning to control levels during the recovery period after CCBC or WCBC. Intracellular pH rose from 7.17+-0.03 to 7.85+-0.05 during CCBC (P<.0005 versus WCBC). MVo2declined dramatically during arrest at either temperature but to a lower value during CCBC (P<.0005). LV pressure recovered to 86.1+-5.1% of its prearrest value after CCBC and to 97.2+-7.8% following WCBC (P=NS). After CCBC but not WCBC, there were small but significant increases in LV end-diastolic pressure (by 1.3 mm Hg, P<.05) and in the LV relaxation constant, tau (from 37.3+-1.5 to 42.3+-2.4 milliseconds, P<.05).Conclusions The increase in intracellular pH during CCBC is largely accounted for by physicochemical factors.Group differences in ATP over time may be related to rapid cooling contracture during CCBC. The data suggest that CCBC mildly impairs LV function but that WCBC preserves function and metabolism at or near prearrest levels. (Circulation. 1994;90 (part 2):II-328-II-338.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Cardiac operations and cardiopulmonary bypass are associated with a host of unphysiological consequences that have widespread systemic effects.Since previous investigations in human cardiac transplant recipients had demonstrated that left ventricular (LV) torsional deformation was a sensitive method to detect subclinical LV dysfunction during acute rejection, we studied LV systolic torsion and diastolic recoil preoperatively and postoperatively in a canine model using myocardial marker techniques.Methods and Results Seven dogs underwent placement of LV subepicardial myocardial markers and creation of mitral regurgitation.Three months later, the animals underwent high-speed, biplane videofluoroscopic analysis for determination of LV systolic function and regional LV systolic torsional deformation and diastolic recoil. The animals then underwent chordal-sparing mitral valve replacement and were restudied 1 to 2 hours postoperatively. One to 2 hours after the cardiac operation, regional maximal systolic torsional deformation decreased significantly in all three LV regions on the lateral LV wall, as well as in the apical and apical-equatorial regions on the anterior wall. During early systole, minimal regional systolic torsion increased significantly in all regions on the lateral wall, as well as in the apical level of the posterior wall. Heterogeneous decreases in torsional deformation were also seen during the early diastolic filling period.Conclusions Regional systolic torsional deformation and diastolic recoil are markedly perturbed early after a cardiac operation and its associated manipulations.Such changes, however, may potentially serve as sensitive tools to assess the impact of different techniques of intraoperative management, includ- ing newer methods of myocardial protection. (Circulation. 1994;90(part 2):II-339-II-346.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background The accuracy of conductance measurement of left ventricular (LV) volume is affected by parallel conductance (Vp) from right ventricular (RV) volume as well as surroundings of the heart.No studies have quantified the extrinsic influences on Vp.Methods and Results In six anesthetized pigs, using a median sternotomy and pericardial well, implantable cardioverter defibrillator patches, normal saline, or echocardiography gel were in-troduced and removed. LV end-diastolic pressure (LVEDP) did not change significantly with these interventions. Raw LV conductance was used to estimate end-diastolic volume (LVEDV), end-systolic volume (LVESV), and stroke volume (SV). Saline significantly increased mean+-SEM calculated LVEDV from 106+-8 to 131+-6 mL and calculated LVESV from 81+-7 to 110+-5 mL; calculated SV decreased from 25+-3 to 21+-2 mL (P<.05, paired t test). Implantable cardioverter defibrillator patches and gel did not significantly change calculated LV volumes. LV conductance was also measured in arrested hearts during LV filling (5 to 60 mL) at four levels of RV volume (RVV). Using a fixed value for Vp, calculated mean LV volume was 30+-3 mL at RVV=0, 32+-3 mL at RVV=20, 33+-3 mL at RVV=40, and 36+-3 mL at RVV=60 (P<.01, repeated-measures ANOVA).Conclusions While implantable cardioverter defibrillator patches and gel have no statistically significant effect, saline and RVV affect LV volume calculations by conductance, requiring special techniques during cardiopulmonary bypass or caval occlusion.(Circulation. 1994;90(part 2):II-347II-352.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID