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The benefits of the automatic DDD (DDD/AMC) mode in the Chorus II pacemaker (Chorus 6234; Ela Medical Inc.), which automatically switches the modes between DDD and AAI to respect spontaneous AV conduction as much as possible in AAI while preserving safety pacing in DDD during paroxysmal AV block (AVB) only, remain unproven. This study examined the functions of the DDD/AMC mode in 12 patients with sick sinus syndrome (SSS; n = 10) or paroxysmal complete AVB (n = 2). A short-term (24 hours) comparative study between simple DDD mode and the DDD/AMC mode was performed in 8 of the 12 patients, and a medium-term (55.2 +/- 54.6 days) follow-up of the DDD/AMC mode was completed in all 12 patients. A comparative pair of 24-hour surface Holter ECGs was obtained in 6 of the 8 patients in the short-term study. Telemetry and built-in Holter histograms were collected in the outpatient clinic in all 12 patients. Although the percentage atrial pacing of the telemetry increased from 59.2 +/- 35.4 in DDD to 70.4 +/- 31.8 in DDD/AMC (P0.009; n = 8), the percentage ventricular pacing decreased from 64.6 +/- 37.7 in DDD to 36.2 +/- 43.1 in DDD/AMC (P0.027) in the short-term study. In particular, the reduction of percentage ventricular pacing to10% was observed in four patients with SSS not associated withor = first-degree (1 degree) AVB on preoperative ECGs. Between the two modes a significant difference in arrhythmic events was not observed by the 24-hour surface Holter ECGS taken from the six patients in the short-term study. AAI-DDD switching associated with automatic modulation of AV delay and AV hysteresis occurred in all patients in the medium-term study. From the medium-term study, the total AV delay (AV delay plus AV hysteresis) exceeded 300 ms in 6 of the 12 patients in DDD/AMC, and usually became longest during nighttime. From the short- or medium-term study in the 12 patients, two patients preferred the DDD/AMC mode while one preferred the DDD mode. These results suggest that the DDD/AMC mode is useful, at least in SSS patients withoutor = 1 degree AVB, by reducing the percentage ventricular pacing.

A retrospective study was conducted on 124 patients who underwent re-replacement of previously implanted prosthetic heart valves for structural valve failure, prosthetic valve endocarditis, periprosthetic leak, a thrombosed valve, hemolysis, or prophylactic removal. In total, 85% of the explanted valves were bioprostheses, and 70% of the newly implanted valves were mechanical valves. The overall operative mortality rate was 8.1%, being 3.2% of 95 single valve recipients and 25.0% of 28 double valve recipients (P < 0.001). The overall mortality rate dropped from 13.6% of 66 patients before 1988, to 1.7 % of 58 patients encountered in the last 3 years (P < 0.02). Since 1988, a third of the patients have undergone reoperation without homologous blood transfusion. A univariate analysis revealed eight operative risk factors, namely: higher values of preoperative blood urea nitrogen or total bilirubin, double valve replacement at the redo operation, NYHA class IV, urgency of reoperation, a duration of implantation of less than 3 months, reoperation in the earlier period of this study, and reexploration for bleeding or cardiac tamponade after re-replacement surgery. A multivariate statistcial analysis demonstrated that preoperative blood urea nitrogen, urgency of reoperation, double valve replacement, and the duration of implantation were independent risk factors. Thus, we recommend that surgery be performed early, before the occurrence of other organ failure induced by congestive heart failure due to any form of valve dysfunction.

The present study was performed to determine whether the effects of ischemic preconditioning are mediated by a decrease in myocardial contractile activity or by a change in catabolite accumulation during the subsequent period of sustained ischemia. In ischemic preconditioning groups, crystalloid perfused rat hearts were subjected to 5 or 10 min of global ischemia before a 15-min reperfusion period and a subsequent 30 min period of ischemia, Non-preconditioned control hearts underwent a single 30-min ischemic period. In the 5-min preconditioned hearts, the onset of myocardial contracture was significantly delayed (22.0 +/- 1.6 min) compared with that in control hearts (14.7 +/- 0.7 min). Tissue ATP content of the myocardium during sustained ischemia was preserved better in 5-min preconditioned hearts than in control hearts. The time to contractile arrest during the sustained ischemic period was greater in the preconditioned hearts (3.9 +/- 0.3 and 3.1 +/- 0.2 min in PC5 and PC10 hearts respectively) than in controls (1.9 +/- 0.1 min). Thus, residual myocardial work during sustained ischemia (as estimated by the rate pressure product) was not decreased in the preconditioned hearts compared with that in control hearts. Extracellular acidosis was identical among the three groups during the subsequent period of sustained ischemia. The early rise in extracellular K+ during sustained ischemia progressively increased with the duration of preconditioning. We conclude that, in crystalloid perfused rat heart, 5 min of global ischemia had a salutary effect against cell damage caused by sustained ischemia. This "preconditioning" effect cannot be attributed to decreased myocardial work during ischemia nor to differences in extracellular H+ or K+ accumulation.

The mitral apparatus can affect left ventricular function through various mechanisms, such as the direct mechanical coupling between the mitral anulus and papillary muscle and the mitral annular contraction. To evaluate the relative contribution of these mechanisms, we investigated in five groups of 35 dogs that underwent open chest operations how preservation of the mitral apparatus affects left ventricular systolic function. We performed atriotomy in the first group. We sutured a prosthetic rigid ring around the mitral anulus in the second group. We replaced the mitral valve and preserved the anterior chordae in the third group, the posterior chordae in the fourth group, and no chordae in the fifth group. The postoperative percentage of recovery of ventricular function (as assessed by the slope of the end-systolic pressure-volume relation) from preoperative control values were 92.2% +/- 4.8%, 89.5% +/- 12.8%, 85.7% +/- 9.5%, 75.1% +/- 12.9%, and 61.3% +/- 8.0%, respectively. Preservation of the mitral apparatus significantly improved left ventricular function compared with that of conventional mitral valve replacement. The average relative contribution of the ventricular muscle to left ventricular function, the mitral anulus-papillary muscle continuity, and the mitral annular contraction were 66.5%, 30.6%, and 2.9%, respectively. We conclude that it is more beneficial to preserve the mitral apparatus in mitral valve replacement. The prosthetic ring does not detract from the functional benefit of the preservation of the mitral apparatus.

To evaluate the effect of tranexamic acid (TA) on blood loss after cardiopulmonary bypass (CPB), 157 patients who underwent elective valve replacement operations were studied, with one group of 90 patients receiving tranexamic acid (Group TA) and 67 patients serving as the control group (Group N). In group TA, 50 mg/kg of tranexamic acid was administered just before and after CPB, and every 90 minutes during CPB. The activated coagulation time was maintained at more than 450 seconds during CPB in both groups. There was no significant difference in the CPB time between the groups (163 +/- 32 min in group N and 152 +/- 38 min in group TA:NS). The time required for hemostasis was shortened in group TA, which resulted in a shorter operation time (6.7 +/- 1.5 hrs vs 6.0 +/- 1.5 hrs in group N and group TA, respectively: p = 0.006). The amount of chest tube drainage within 12 hours after surgery was significantly reduced (225 +/- 129 ml vs. 180 +/- 118 ml in group N and group TA, respectively: p = 0.026). The chest tube was able to be removed earlier in group TA, and the total blood loss was significantly smaller in group TA (402 +/- 292 ml) than in group N (631 +/- 609 ml; p = 0.004). The authors thus conclude that antifibrinolytic therapy during CPB with tranexamic acid reduces postoperative blood loss, and shortens the operation time due to an improvement in hemostasis.

From February 1975 to August 1981, 23 consecutive patients underwent tricuspid valve replacement, which was either isolated (six patients) or combined with the replacement of other valves (17) by means of a standard, glutaraldehyde-preserved Hancock porcine bioprostheses. Patients’ ages ranged from 9 to 53 (mean 36.2) years. The follow-up period ranged from 0.2 to 16.5 years (mean 9.1) and was complete in 100 % of all cases. Structural valve failure of the tricuspid Hancock valve was noticed in two patients, a 9-year-old boy and a 13-year-old girl 3.4 and 16.5 years after implantation, respectively. The actuarial freedom rate from structural valve failure at 10 years was 94 ± 6 %. There were six tricuspid prosthesis-related events: structural valve failure in two and valve thrombosis, anticoagulant-related bleeding, prosthetic valve endocarditis, and periprosthetic leak in one each, respectively. The actuarial freedom from these events at 10 years was 78 ± 10%. Five pairs of aortic/mitral-tricuspid Hancock valves were explanted simultaneously from the same patients after 8.1 to 13.9 (mean 11.4) years postoperatively. A gross examination showed no valve dysfunction in the explants from the tricuspid position, but degenerative changes with valve dysfunction in those from the mitral and aortic position were observed (none of five versus five of seven; p

The following hypotheses were tested using an isolated perfused working rat heart model: (1) Collins' solution for cold storage of the heart is harmful for the heart during reperfusion; (2) a "reverse" of the intracellular-type Collins' solution with an extracellular-type cardioplegic solution before reperfusion is able to prevent this disadvantage of Collins' solution. The following two major groups (I and II) and five subgroups (-a to -e) in each group were prepared. In group I (reversed group); the hearts were initially stored in Collins' solution but were reversed by a 1-minute flush with cardioplegic solution followed by storage in cardioplegic solution for the last 1 to 180 minutes of the total 3-hour storage, that is, groups I-a (reversed for 1 minute), I-b (10 minutes), I-c (30 minutes), I-d (90 minutes), and I-e (180 minutes). In group II (nonreversed control group); the hearts were stored in Collins' solution throughout 3 hours and were also divided into five subgroups of groups II-a, II-b, II-c, II-d, and II-e in which only a 1-minute flush with Collins' solution was performed at the point corresponding to group I. The coronary flow in any of group II showed a marked decrease during the early reperfusion period. In group I, however, the coronary flow increased significantly in proportion to the duration of the reversing phase. The recovery of the aortic flow and the cardiac output in group I showed a bell-shaped pattern in relation to the duration of the reversing phase, reaching their peak values when reversed for 30 minutes (group I-c). The prolonged reverse (180 minutes) resulted in a deterioration of functional recovery associated with a poorer preservation of high-energy phosphates and a larger enzyme leakage. These results suggest that the beneficial effects of intracellular-type Collins' solution for cold storage of the heart were further improved by reversing Collins' solution with the extracellular-type cardioplegic solution for the last 30 minutes of the 3-hour cold storage because the disadvantageous vasoconstriction due to Collins' solution during reperfusion was successfully prevented by the replacement of intravascular and extravascular Collins' solution with cardioplegic solution before the reperfusion.

Objective: The aim was to investigate the effects of a calcium antagonist (diltiazem) and a catecholamine (noradrenaline) on extracellular potassium accumulation during global ischaemia. Methods: Extracellular potassium concentration ([K+]e) was measured during 30 min global ischaemia in the isolated rat heart using a valinomycin potassium sensitive electrode. Contracture development during ischaemia was measured throughout with an intraventricular balloon inserted into the left ventricle and myocardial adenine nucleotides were measured in separate series of hearts. Results: In control hearts, [K+]e showed a characteristic triphasic change during 30 min global ischaemia. This consisted of an early rising phase followed by a transient falling phase after the initial peak of [K+]e, and then a late rising phase. Diltiazem suppressed the rate of rise of [K+]e during early ischaemia, but extended the time course of the early [K+]e rise with the higher dose, abolishing the transient falling phase of [K+]e. During late ischaemia, the rise in [K+]e was attenuated by diltiazem. Noradrenaline also suppressed the early extracellular potassium accumulation, but in contrast to diltiazem, hastened the time course of the late [K+]e rise. Conclusions: Although diltiazem suppresses the early potassium loss during ischaemia as previously described, the drug also decreases the [K+]e fall by some as yet unknown mechanism, so that the [K+]e level becomes higher than control during the falling phase. Cardiovascular Research 1992; 26 :1040-1045

Mechanisms and kinetics of the effects of the ionic composition of two different storage solutions, an intracellular type and an extracellular type, were analyzed by examining the myocardial functional and metabolic recovery processes during the early reperfusion periods after 3 hours of cold storage using an isolated perfused working rat heart model. The hearts were stored either in our own cardioplegic solution (group 1) or in Collins’ solution (group 2) for 3 hours at 4° C and were then reperfused. The electromechanical activity in group 1 was elevated, as indicated by a higher incidence of ventricular fibrillation at 5 minutes of reperfusion (group 1: 5/6; group 2: 0/5; p horac C ardiovasc S urg 1992;104:1320-8)

To assess the underlying mechanisms of ventricular fibrillation induced by myocardial reperfusion after cardioplegic arrest, 62 patients undergoing an open heart operation were divided into two groups based on the absence (group 1, n = 37) or the development (group 2, n = 25) of reperfusion-induced ventricular fibrillation. There was no close relationship between the incidence of reperfusion-induced ventricular fibrillation and aortic clamp time. On reperfusion, the time to onset of cardiac activity was similar in groups 1 (2.4 +/- 1.8 minutes) and 2 (1.9 +/- 1.1 minutes). At that time, there was no significant difference in values of arterial oxygen and bicarbonate contents, pH, or base excess between the two groups, but myocardial temperature was significantly higher in group 2 (25.6 degrees +/- 3.4 degrees versus 27.6 degrees +/- 2.4 degrees C; p less than 0.05). In addition, serum levels of sodium (123.9 +/- 4.2 versus 126.1 +/- 3.7 mmol/L; p less than 0.05) and calcium (0.80 +/- 0.07 versus 0.84 +/- 0.05 mmol/L; p less than 0.05) were significantly higher and serum potassium levels (3.98 +/- 0.58 versus 3.55 +/- 0.61 mmol/L; p less than 0.02) and the serum potassium to calcium ratio (4.94 +/- 0.90 versus 4.29 +/- 0.72; p less than 0.01) significantly lower in group 2. Postoperative serum levels of the myocardial-specific isoenzyme of creatine kinase and myoglobin were similar in both groups. By multivariate analysis, shorter ischemic time, higher myocardial temperature, higher serum sodium concentration, and lower serum potassium to calcium ratio were found to influence induction of reperfusion-induced ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

大動脈弁と僧帽弁の二弁置換症例を対象に, 心筋保護液の順行性投与 (Ante) 法と逆行性投与 (Retro) 法の心筋保護効果を比較した. Ante 群15例, Retro 群 (Ante 法併用 Retro 法) 13例について, 術前および術中因子, 再灌流後CPK-MB値の推移, 術周期心筋梗塞の頻度, 術後血行動態を検討した. 術前因子は両群間に差を認めなかった. 大動脈遮断中の心筋保護液投与の間隔は Ante 群29.2±4.8分, Retro 群24.0±3.8分と Retro 群にて有意に (p

Continuous intravenous infusion of chlorpromazine (CPZ) was used for both sedation and after-load reduction in 13 Japanese patients (Group 1) supported by an intraaortic balloon pump (IABP) after open-heart surgery. CPZ was initiated at a dose of 0.05 mg/kg/hr and was maintained in an approximate dose range of 0.1-0.3 mg/kg/hr depending on individual patient needs. The drug was administered until the IABP was removed and the blood gases were normalized. During this period, the patients slept well and the trigger lines for the IABP were sufficiently secured. In order to evaluate the hemodynamic changes in these patients, the 10 patients who were supported by the IABP and given continuous intravenous sodium thiamylal (ST) for sedation in an approximate dose range of 1-2 mg/kg/hr (Group 2) were employed as controls. After administration of CPZ, the systemic vascular resistance, central venous pressure, and left atrial pressure decreased, while the cardiac output increased. The predicted untoward effects of CPZ, such as tachycardia and hypotension, were minimal. In the ST group, by contrast, the cardiac output decreased somewhat in association with the increase in systemic vascular resistance. From these results, we conclude that constant intravenous CPZ is beneficial for postcardiotomy patients who have severe low cardiac output syndrome and are supported with IABP, by both successfully sedating the patients and reducing ventricular afterload.

Left ventricular hypertrophy has been reported after ascending aorta-abdominal aorta bypass, despite seemingly insignificant changes in cardiac output and mean arterial pressure. Such a bypass procedure may be used for the treatment of complex coarctation of the aorta, hypoplastic aortic arch, or thoracoabdominal aortic aneurysm. To investigate the effect of the bypass procedure on left ventricular afterload, we measured aortic input impedance in six open chest dogs by placing a knitted Dacron graft from the ascending aorta to the abdominal aorta and occluding the aortic arch. Cardiac output and mean arterial pressure remained unaltered throughout the experiment, consistent with clinical reports. Systolic pressure increased by 25% of control, and the ratio of diastolic pressure-time index to tension-time index decreased by 27%. The measured input impedance was then approximated with the three-element windkessel model, which consists of resistance, compliance, and characteristic impedance (average of impedance modulus between 5 and 15 Hz). There was no change in resistance and compliance; characteristic impedance increased to 255% of control. Connecting an air chamber to the vascular prosthesis doubled the compliance and decreased the characteristic impedance nearly to the control value without altering resistance. It also reduced the systolic pressure by 14% of the bypass protocol and increased the ratio of diastolic pressure-time index to tension-time index (by 32% of control value and 82% of bypass value). Arterial systolic pressure and pulse pressure were both linearly correlated with the characteristic impedance. Thus we conclude that although ascending aorta–abdominal aorta bypass does not affect cardiac output, mean arterial pressure, resistance, or compliance, it does increase characteristic impedance. Left ventricular systolic load is directly correlated with characteristic impedance. Increased systolic wall stress might be the cause of left ventricular hypertrophy of the previously reported cases. Because decrease in the distensibility of the proximal aorta is one of the factors causing the increase in characteristic impedance, using a compliant graft might help to unload the heart.

Postoperative changes in serum myoglobin levels have been studied in 47 patients undergoing open heart surgery. The patients were retrospectively divided into two groups according to the time to peak myoglobin level during reperfusion. In 38 patients, myoglobin levels increased rapidly to a peak within 3 hours after reperfusion, after which it was cleared from the blood (group 1). Contrarily, a rise in myoglobin levels was persistent for 24 hours and its time to peak was greater than 3 hours after reperfusion in nine patients (group 2). There were no differences in preoperative and early reperfusion (within 1 hour of reperfusion) values of myoglobin between the two groups. At 3, 6, and 12 hours of reperfusion, myoglobin levels were significantly greater in group 2: 448 +/- 196 vs 1,149 +/- 900 ng/ml, 359 +/- 172 vs 2,653 +/- 3,179 ng/ml, 184 +/- 95 vs 1,896 +/- 1,387 ng/ml, respectively, p less than 0.0001 in each. The maximum activities of both myoglobin and CK-MB were significantly higher in group 2 (myoglobin-max: 771 +/- 257 vs 3,221 +/- 3,024 ng/ml, p less than 0.0001; CK-MBmax: 107 +/- 60 vs 227 +/- 219 IU/L, p less than 0.005). Five of nine patients in group 2 required post-operative assistance with intra-aortic balloon pumping (p less than 0.0005 compared with one of 38 in group 1) and perioperative myocardial infarction developed in three patients (33.3 percent) in this group (p less than 0.005 compared with 0 percent in group 1). Thus, patients with a delayed peak of serum myoglobin level exhibited detrimental cardiac failure postoperatively. These findings suggest that myocardial injury accelerated by reperfusion following ischemia might progress in these patients.

The protective effect of low-calcium, magnesium-free potassium cardioplegic solution on ischemic myocardium has been assessed in adult patients undergoing heart operations. Postreperfusion recovery of cardiac function and electrical activity was evaluated in 34 patients; 16 received low-calcium, magnesium-free potassium cardioplegic solution (group I) and 18 received St. Thomas’ Hospital solution, which is enriched with calcium and magnesium (group II). There were no significant differences between the two groups in age, sex, body weight, and New York Heart Association functional class. Aortic occlusion time (107.3 ± 46.8 minutes versus 113.6 ± 44.3 minutes), highest myocardial temperature during elective global ishemia (11.5° C ± 3.1° C versus 9.3° C ± 3.2° C), and total volume of cardioplegic solution (44.2 ± 20.5 ml/kg versus 43.4 ± 17.6 ml/kg) were also similar in the two groups. On reperfusion, electrical defibrillation was required in four cases (25.5%) in group I and in 15 cases (83.3%) in group II (p

To evaluate the effects of pericardial meshing (multiple incisions on the pericardium) on cardiac function, we examined left ventricular pump performance before and after pericardial meshing in six open chest dogs. We evaluated left ventricular systolic properties with the slope of end-systolic pressure-volume relation and diastolic properties with end-diastolic pressure-volume relation (chamber compliance). Overall left ventricular performance was assessed with end-diastolic pressure versus cardiac output relation. Left ventricular chamber compliance was increased (31.3%) with pericardial meshing compared with direct closure of the pericardium, and cardiac output was increased (26.7%) for any given left ventricular end-diastolic pressure. The slope of the end-systolic pressure-volume relation was not altered in pericardial meshing. These results suggest that pericardial meshing improves left ventricular pump performance as a result of increasing left ventricular chamber compliance. This technique may benefit cardiac pump performance that is depressed by the direct closure of the pericardium after cardiac operations.

We report a case of a 40-year-old man who had a quadricuspid aortic valve associated with aortic regurgitation. The anomaly was revealed by transesophageal echocardiography (TEE), and confirmed by cardiac surgery. TEE is a useful noninvasive method for identifying the quadricuspid aortic valve.

Hemoconcentration for the establishment of no-donor blood transfusion in open heart surgery was assessed in regard to both the saving of protein and platelets and the exclusion of free hemoglobin. Two different types of hemoconcentrator were compared: the ultrafilter (group I, 6 patients) and the Cell Saver (group II, 6 patients). The total serum protein level, expressed as the percent recovery of the preoperative value, after hemoconcentration was significantly higher in group I (group I versus group II: total serum protein, 118% versus 87% [p less than 0.05]; fibrinogen, 77% versus 50% [p less than 0.01]; immunoglobulin, 83% versus 60% [p less than 0.01]). The platelets also seemed to be well preserved after hemoconcentration in group I. Although the exclusion of free hemoglobin from plasma was inferior in group I compared with group II, the postoperative plasma free hemoglobin level did not increase in group I. We conclude that use of the Cell Saver in nontransfusion cardiopulmonary bypass might cause a severe depletion of various proteins and that the ultrafilter is both safer and more useful if employed routinely.

Although left heart bypass has gained popularity as a powerful technique to assist the severely failed left heart, apparent right heart failure has often developed during the bypass procedure. We investigated whether the coexisting right heart failure is attributable to the left heart bypass in 16 open-chest dogs. We evaluated the effects of left heart bypass on the right ventricular systolic properties by the slope of the end-systolic pressure-volume relation and its effects on the diastolic properties by chamber compliance. Overall right ventricular performance was assessed by the end-diastolic pressure versus cardiac output relationship. The left heart bypass decreased the slope slightly when the assisted flow ratio exceeded 75% (‘-14% ±8% at the assisted flow ratio of 100%, p

Retrograde administration of cardioplegic solution via the right atrium with continuous cooling of the right ventricular cavity (right atrial perfusion cooling) was assessed for its protective effect in 12 dogs with occlusion of the right coronary artery subjected to global ischemia for 60 minutes. After an initial administration of 4° C crystalloid cardioplegic solution by antegrade aortic perfusion, myocardial protection was established either by right atrial perfusion cooling (group I; n = 6) or by antegrade aortic perfusion alone (group II; n = 6). The right ventricular temperature was approximately 15° C in group I and 20° C in group II. After ischemia for 60 minutes, the adenosine triphosphate content of the right ventricular free wall was significantly higher in group I than in group II (24.4 ± 1.45 versus 13.8 ± 234 μmol/gm dry weight, p

Comparative long-term performance characteristics of mechanical valves and bioprosthetic valves were analyzed retrospectively for patients who had undergone isolated mitral valve replacement from 1967 to 1988. Two hundred ninety-one patients received either mechanical (n = 97) or bioprosthetic (n = 194) valves. The cumulative follow-up was 1,609 patient-years (mean 6.3 +/- 3.8 years, ranging from 0.6 to 20.2 years, 98.9% complete follow-up). The actuarial survival rate, including hospital deaths, at 10 years was 72 +/- 12% for mechanical and 74 +/- 4% for bioprosthetic valve recipients. The rates of freedom from thromboembolism, structural valve failure, prosthetic valve endocarditis, prosthetic valve endocarditis, reoperation, and overall valve-related complications at 10 years were 87 +/- 5%, 100%, 91 +/- 3%, 100%, and 79 +/- 8% for mechanical valve recipients and 85 +/- 3%, 77 +/- 5% (p less than 0.001), 85 +/- 13%, 71 +/- 5% (p less than 0.001), and 52 +/- 5% (p less than 0.001) for bioprosthetic valve recipients, respectively. Thromboembolism occurred at a similar incidence in two types of valves (2.0 +/- 0.7 vs. 2.2 +/- 0.4%/pt-yr). Structural valve failure, reoperations, and overall valve-related events occurred more frequently in the bioprostheses recipients (0 vs. 2.0 +/- 0.4%/pt-yr; p less than 0.001, 0.3 +/- 0.3 vs. 2.9 +/- 0.5%/pt-yr; p less than 0.001, 2.5 +/- 0.8 vs. 5.6 +/- 0.7%/pt-yr; p less than 0.005, respectively). There was no mortality at the time of redo-operation. These results show that bioprostheses in the mitral position exhibit small benefits of antithrombogenesis and prominent disadvantage of poor durability requiring reoperation.

Comparative long-term performance characteristics of mechanical valves and bioprosthetic valves were analyzed retrospectively among patients who had undergone isolated aortic valve replacement between 1968 and 1987. One hundred sixty-seven patients received either mechanical (n = 82) or bioprosthetic (n = 85) valves. The cumulative follow-up was 926 patient-years (mean 6.1 +/- 4.7 years, ranging from 0.5 to 20.2 years, 100% complete follow-up). Actuarial survival rate, including operative death, at 10 years was 74 +/- 7% for mechanical and 77 +/- 7% for bioprosthetic valve recipients. The rates of freedom from thromboembolism, structural valve failure, prosthetic valve endocarditis, and valve re-replacement at 10 years were 77 +/- 7%, 100%, 96 +/- 2% and 95 +/- 3% for mechanical, and 94 +/- 4%, 83 +/- 8% (p less than 0.05), 88 +/- 5% and 75 +/- 8% (p less than 0.05) for bioprosthetic valve recipients, respectively. Thromboembolism occurred more frequently in the mechanical valve recipients (p less than 0.01), and structural valve failure in the bioprostheses recipients (p less than 0.05). There was no mortality at the time of valve re-replacement. Most of the bioprosthesis recipients received no anticoagulation therapy beyond 3 months postoperatively. Cardiac medication in the late postoperative period was not required in 31.3% of bioprosthetic, and 3.2% of mechanical valve recipients (p less than 0.01). These results show that bioprosthesis in the aortic position exhibits a superb antithrombogenicity and may enable a drug-free state, though its limited durability requires reoperation.

Objective: Correlations and risk factors remain to be unclarified for post-heart-surgery posttransfusion graft-versus-host disease, mediastinitis, and late cardiac tamponade caused by deteriorated host-defense mechanisms due to cardiopulmonary bypass both with and without steroid usage.Methods: We sent questionnaires to 298 Japanese cardiovascular institutions asking for institution profiles, including infection control, steroid use in cardiopulmonary bypass, and prevalence of mediastinitis, late cardiac tamponade, and posttransfusion graft-versus-host disease during 1994. The overall prevalence of posttransfusion graft-versus-host disease since the start of service (from establishment of institution to date) was also requested.Results: The number of pump cases at the 119 institutions responding (40%) were 91.6±67.9 cases/institution (total = 10,904). The prevalence of mediastinitis was 1.2±1.8 and that of late cardiac tamponade 1.0±1.8%. Posttransfusion graft-versus-host disease occurred in 1 of 10,904 patients (0.01%) during 1994 at an institution where steroids and nonirradiated blood were used in surgery. The simple institutional mean prevalence of posttransfusion graft-versus-host disease since establishing institutions was 0.08±0.13%. Of the 119 institutions surveyed, 86 used steroids in all pump cases (72%); 11 institutions used steroids in a limited number of cases (9%). The institutional mean of methylprednisolone-converted steroid dose was 21.5±16.4 mg/kg (n = 119). In multivariate regression analysis, operation time (p=0.005) for mediastinitis, steroid usage (all, limited, or no cases) (p=0.01) and %aneurysm (p=0.05) for late cardiac tamponade, and steroid dosage (p=0.002) for posttransfusion graft-versus-host disease were identified as significant risk factors.Conclusion: Our results suggest that massive steroid administration for cardiopulmonary bypass may increase the risk of posttransfusion graft-versus-host disease and late cardiac tamponade, but not mediastinitis.

We investigated the protective effects of succinate, which is a respiratory substrate and a potential antioxidant, on myocardial ischemia/reperfusion injury with the whole heart. Isolated rat hearts were loaded with 25-min normothermic global ischemia followed by 30-min reperfusion in a working heart model. Succinate administered either before reperfusion or added to the cardioplegic solution improved the postischemic cardiac function significantly. The hearts arrested with succinate-supplemented cardioplegic solution replenished high-energy phosphates and maintained the total adenine nucleotides during the reperfusion period, whereas those arrested with succinate-nonsupplemented cardioplegic solution replenished the high-energy phosphates less, and also lost total adenine nucleotides during that period. We thus conclude that succinate administered before reperfusion may decrease the degree of mitochondrial damage during reperfusion and thereby reduce the amount of myocardial ischemia/reperfusion injury.

Protamine sulfate often causes hypotension during heparin neutralization. The concept of ventricular-arterial coupling was applied to determine whether a negative inotropic effect or a vasodilating effect of protamine was the major contributing factor to this hypotension. Thirty-five patients who underwent cardiac operations were studied during operation by measuring instantaneous left ventricular pressure and aortic flow to examine the end-systolic pressure-volume relationship. We obtained end-systolic elastance and effective arterial elastance values in a beat-to-beat fashion with a single-beat estimation method. In 28 of the 35 patients (80%), mean arterial pressure decreased more than 10 mm Hg with protamine infusion. Parameters were compared at the following three points: before a decrease in mean arterial pressure (control), at maximally decreased mean arterial pressure (maximum), and at a middle point between control and maximum values (midpoint). At both midpoint and maximum, mean arterial pressure decreased significantly (control 79.6 ± 12.6 mm Hg, midpoint 66.5 ± 10.8 mm Hg, maximum 52.7 ± 9.9 mm Hg; p < 0.01). Similar changes were observed in effective arterial elastance (control 2.00 ± 0.75 mm Hg/ml, midpoint 1.60 ± 0.53 mm Hg/ml, maximum 1.31 ± 0.46 mm Hg/ml; p < 0.01). Although the decrease in end-systolic elastance at midpoint (control 3.08 ± 1.61 mm Hg/ml, midpoint 2.92 ± 1.68 mm Hg/ml) did not reach statistical significance, end-systolic elastance significantly decreased at maximum (2.63 ± 1.46 mm Hg/ml; p < 0.01). Continuous measurements showed that the decreases in mean arterial pressure and effective arterial elastance always preceded the depression of end-systolic elastance and that afterload reduction by vasodilating effect of protamine was the mechanism most likely to have initiated the hypotension. Delayed decrease in contractility may be ascribed to reduced coronary perfusion pressure caused by vasodilation or to a direct effect of protamine. (J Thorac Cardiovasc Surg 1996;112:462-71)

To examine the correlation between the size of left atrial myxoma, the degree of pulmonary hypertension and the patient's New York Heart Association (NYHA) functional class, the records of 29 surgically treated patients with left atrial myxoma were reviewed. Of 29 patients, 23 were catheterized before surgery. As the preoperative NYHA functional class advanced, the preoperative mean pulmonary artery pressure (mmHg) was seen to increase. Moreover, the weight of the excised myxoma also correlated well with the preoperative pulmonary artery pressure value. In five patients inserted with a Swan-Ganz catheter, the mean pulmonary artery pressure decreased immediately after tumour excision. Postoperatively, the average NYHA class of the 29 patients significantly improved. These results confirmed the positive correlation between the size of the tumour, the pulmonary artery pressure, and NYHA class in patients with left atrial myxoma.

A simplified Manouguian's aortic annular enlargement for aortic valve replacement with prosthetic valve was performed in a patient with severe aortic stenosis and mild regurgitation by preserving both the anterior mitral leaflet and the left atrial roof intact. This method minimized the operative risk by avoiding injury to the mitral valve, while inserting a possibly two-size-larger prosthetic valve. The inserted prosthetic valve was positioned parallel to the original aortic valve. Moreover, the incision from the top of the commissure between the non-coronary cusp and left coronary cusp through the interventricular fibrous trigone appears to be easily extended into the exact center of the anterior mitral leaflet if further enlargement is required.

A case of active prosthetic valve infective endocarditis (PVE) due to Candida glabrata was successfully treated by the systemic administration of fluconazole. A 66-year-old Japanese man with infective endocarditis of unknown etiology underwent aortic and mitral valve replacement to treat severe aortic and mitral regurgitation associated with multiple organ failure. Postsurgical cultures of arterial blood were repeatedly positive for C. glabrata, and therefore fluconazole was administered either intravenously or orally at a dose of 400 mg/day for 46 days. During that time the signs of inflammation including fever such as an elevated white blood cell count and the presence of C-reactive protein (CRP) all improved while the blood cultures became negative. Fluconazole is thus considered to be effective in treating PVE caused by C. glabrata. When administering this treatment, it is also important to monitor the patient's renal and liver function.

Although Manouguian's operation is well established, there have been little long-term data published on its outcome. From January 1980 to June 1988, 15 patients underwent patch enlargement of the small aortic anulus by Manouguian's approach, either with aortic single valve replacement (7 patients) or with aortic-mitral double valve replacement (8 patients). Follow-up ranged from 3.0 to 11.4 years (mean 8.5) and was completed with a cumulative total of 102 patient-years. One patient died of fulminant hemolysis, probably related to turbulent jet flow and Dacron patch material (operative mortality 6.7%). There were four late deaths, and the actuarial survival, including operative death at 10 years, was 62% +/- 14%. Reoperations were performed seven times in six patients. Most of these complications were not considered to be caused by the anulus-enlarging procedure. Actuarial freedom rate from reoperation at 10 years was 65% +/- 15%. Four patients underwent rereplacement of prostheses for Hancock valve failure during 2.9 to 11.3 years (mean 8.2 years). The anulus enlargement was found to be well healed and presented no problem during reoperation. Surgically induced mitral regurgitation by Manouguian's procedure was observed in two patients. The regurgitation did not progress during follow-up duration of 1.9 to 10.0 years, nor did it cause congestive heart failure. Annular enlargement by Manouguian's procedure with use of mechanical valves is one of the good selections in patients with the narrow aortic valve ring.

From February 1975 through October 1981, 256 Hancock porcine bioprostheses (JohnsonJohnson Cardiovascular, King of Prussia, Pa.) (60 aortic, 169 mitral, and 27 pulmonary/tricuspid position) were implanted in 220 patients (104 male and 116 female, aged 9 to 67 years; mean 43.3) at Kyushu University Hospital in Japan. The procedures include 41 aortic valve replacements, 121 mitral valve replacements, 4 pulmonary valve replacements, 6 tricuspid valve replacements, and 48 combined valve replacements (31 aortic plus mitral, 13 mitral plus tricuspid, and 4 aortic plus mitral plus tricuspid). Hospital mortality was 6.4%. Follow-up was 98% during 8 to 14 (mean 10.5) years. Cumulative follow-up was 1836 patient-years and 2078 valve-years. At 10 years the overall actuarial survival rate, including hospital morality, was 70% +/- 3%, and freedom from valve-related mortality with sudden death was 87% +/- 3%. More than half of the current survivors required no anticoagulant therapy. Freedom from thromboembolism or anticoagulant-related hemorrhage (or both) and prosthetic valve endocarditis was common. Freedom from structural valve failure and reoperation declined more than 9 years after replacement of left-sided heart valves but not after replacement of right-sided heart valves. Sixty-seven patients underwent 68 repeat operations, and there were four deaths (5.9%). The rate of freedom from overall valve-related complications at 10 years was 62% +/- 8% for aortic valve replacement, 53% +/- 5% for mitral valve replacement, 80% +/- 13% for pulmonary/tricuspid valve replacement, and 42% +/- 9% for combined valve replacement. There was a significant difference between pulmonary/tricuspid valve replacement and combined valve replacement (p less than 0.05). The Hancock bioprosthesis is suitable for the replacement of valves in the right side of the heart but not for combined valve replacement.

We examined influences of a blocker (glibenclamide) and an opener (nicorandil) of the ATP-sensitive potassium (KATP) channel on extracellular K concentration [( K+]e), as well as the myocardial function and metabolites during global ischemia and reperfusion in Langendorff-perfused rat heart preparation. In control hearts, [K+]e began to rise 20 s after the onset of ischemia up to an initial peak (8.3 +/- 0.3 mM) at 2.5 +/- 0.7 min, then fell to 6.0 +/- 0.8 mM after 8.2 +/- 0.7 min, and then rose progressively to 14.6 +/- 0.8 mM at the end of 30 min of ischemia. Glibenclamide (50 microM) reduced the initial peak of [K+]e to 7.2 +/- 0.3 mM (P less than 0.01), and nicorandil (200 microM) increased it to 9.4 +/- 0.6 mM (P less than 0.01). There were no significant differences in [K+]e values among all groups at the end of ischemia. During ischemia, nicorandil decreased the time to mechanical arrest from 1.9 +/- 0.1 min to 1.5 +/- 0.1 min, whereas it was increased by glibenclamide to 2.7 +/- 0.4 min. In control hearts, the time to onset of ischemic contracture was 14.7 +/- 1.8 min. Nicorandil delayed onset of contracture and glibenclamide accelerated it. Thus we have confirmed that some part of the early increase in [K+]e during ischemia is attributable to K+ efflux through the KATP channel in our model, and opening of the KATP channel may contribute to a rapid reduction of the contractility of the ischemic myocardium that subsequently protects the myocardium against further ischemic injury.

Comparative long-term performance characteristics of St. Jude Medical (SJM) and bioprosthetic valves were conducted retrospectively for patients who underwent prosthetic valve replacement in the right side of the heart from 1975 to 1988. Fifty-four patients received either SJM (n = 18) or bioprosthetic (n = 37) valves. The cumulative follow-up for SJM valves was 91 valves-years (range 3.9 to 7.2 years) and that for bioprostheses was 282 valve-years (range 1.3 to 14.8 years). Follow-up rate was 100%. The actuarial survival rate excluding hospital deaths at 5 years was 81 +/- 10% for SJM and 97 +/- 3% for bioprosthetic valve recipients (p = ns). The rates of freedom from thrombosis or anticoagulant-related hemorrhage, structural valve failure, prosthetic valve endocarditis, reoperation, and overall valve-related complications at 5 years were 72 +/- 11%, 100%, 100%, 83 +/- 9%, and 72 +/- 11% for SJM valve recipients, and 100%, 97 +/- 3%, 97 +/- 3%, 94 +/- 4%, and 94 +/- 4% for bioprosthetic valve recipients, respectively. Structural valve failure, prosthetic valve endocarditis and reoperations occurred at a similar incidence in each of the two types of prostheses. Thrombosis and overall valve-related events occurred more frequently in SJM valve recipients (5.5 +/- 2.5 vs 0%/valve-year; p less than 0.02, 6.6 +/- 2.7 vs 1.1 +/- 0.6 %/valve-year; p less than 0.03, respectively). The bioprosthetic valve which did not need warfarin anticoagulation therapy had low incidence of valve-related complications and showed good long-term durability even in the younger age group. The bioprosthetic valve was superior to the SJM valve in the right side of the heart.

From May 1975 through December 1988, 91 patients (mean age 50.4 +/- 12.8 years) had first-time surgery for mitral pure regurgitation; 48 had mitral valve replacement (MVR) and 43 had valve repair. A majority of the patients had non-rheumatic valvular diseases. Those patients who underwent repair had less hemodynamic and functional derangement than those who underwent MVR. The operative mortality was 8.3% in the MVR group and 2.3% in the repair group. Seventeen percent of the MVR group and 2% of the repair group required intra-aortic balloon pumping support (p less than 0.03). A higher dose of dopamine and/or dobutamine during the early postoperative period was necessary in the MVR group (7.0 +/- 4.8 micrograms/kg/min) than in the repair group (5.1 +/- 3.1 micrograms/kg/min). Duration of respirator support for hospital survivors was longer in the MVR group (2.3 +/- 2.7 days) than in the repair group (1.4 +/- 1.0 days). There were 5 late deaths (2.2 +/- 1.0%/pt-yr) not counting 6 non-cardiac deaths in the MVR group and 1 (0.6 +/- 0.6%/pt-yr) in the repair group. There were 17 patients (7.5 +/- 1.8%/pt-yr) who experienced treatment failure in the MVR group and 5 (2.3 +/- 1.3%/pt-yr) in the repair group (p less than 0.02). Eight patients in the MVR group (3.5 +/- 1.3%/pt-yr) underwent repeat surgery in the late postoperative period, as did 3 (1.7 +/- 1.0%/pt-yr) in the repair group. There was no increase in the incidence of repeat surgery after valve repair. All the current survivors in the repair group, and 96% of those in the MVR group were in NYHA functional class I or II. These results indicate that mitral repair is the preferred operative procedure for pure mitral regurgitation, whenever it is possible.

A retrospective study of 161 consecutive patients undergoing mitral valve replacement with or without other valve surgery was undertaken to examine the relation between cardiac cachexia and postoperative acute renal failure. The preoperative nutritional state was assessed according to percent of the ideal body weight (W/IW). There were 37 malnourished patients (W/IW less than 0.80) and 124 normally nourished patients (W/IW greater than or equal to 0.80). In nineteen in the malnourished group (51 per cent) and 37 of normal-nourished (28 per cent), postoperative acute renal failure developed. Malnourished patients showed a severe clinical picture preoperatively and complicated operative procedures had to be carried out. To match these clinical factors between the two groups, the observation was limited to the high risk patients who showed severe New York Heart Association Functional Class (III or IV) large cardiothoracic ratio (more than 65 per cent), and long cardio-pulmonary bypass time (exceeding 120 minutes). Even in this subgroup, malnourished patients were susceptible to renal failure (64 per cent versus 20 per cent, malnourished versus normal-nourished respectively). Thus, when malnutrition is superimposed on diminished cardiac performance, acute renal failure may ensue.

As cardiopulmonary bypass is frequently accompanied by hypotension, the effect of varying perfusion pressure (30, 60, and 90 mm Hg) on the adequacy and distribution of coronary flow was studied under conditions of a normothermic beating empty state, of normal and hypertrophied hearts of 20 mongrel dogs, using the radioactive microsphere technique. In the normal hearts, 30 mmHg caused a 47% (P < 0.005 to prebypass) reduction of left ventricular coronary flow but did not change flow distribution (ENDO/EPI flow ratio: 1.01); increasing mean perfusion pressure from 30 to 90 mm Hg did not alter the oxygen consumption but did increase the coronary flow and decrease the oxygen extraction ratio. In the hypertrophied hearts, 30 and 60 mm Hg perfusion pressures resulted in a redistribution of flow away from the subendocardium (ENDO/EPI flow ratio: 0.82 and 0.87, respectively, P < 0.02 to prebypass). An increase in perfusion pressure from 30 to 60 mm Hg resulted in a significant increase in oxygen uptake (4.0 vs 5.6 cc/100 g/min, respectively, P < 0.02). An increased perfusion pressure of 90 mmHg resulted in a sufficient subendocardial flow and an augmentation of the oxygen uptake. These results indicate that subendocardial underperfusion occurs in the beating empty hypertrophied heart, under conditions of lower perfusion pressures (30 and 60 mm Hg), but that such can be improved by increasing the perfusion pressure to 90 mmHg. In contrast, the subendocardial underperfusion does not occur with a perfusion pressure of 30 mm Hg in normal hearts.

A decreased diastolic slope (EF slope) of the tricuspid valve on the M-mode echocardiogram may not indicate the presence of tricuspid stenosis (TS). To explore diagnostic echocardiographic signs of TS, we examined an M-mode and 2-dimensional (2-D) echocardiogram in 9 patients with documented TS of rheumatic origin and in 14 patients with rheumatic heart disease who showed a decreased EF slope (less than 40 mm/s) but did not have TS. By M-mode echocardiography, the EF slope was not different between patients with TS (24.4 +/- 2.2 mm/s) and those without TS (27.4 +/- 2.0 mm/s). The early diastolic excursion (DE amplitude) of the tricuspid valve was significantly lower (p less than 0.001) in patients with TS (7.6 +/- 1.0 mm) than in patients without TS (13.9 +/- 0.6 mm). Two-dimensional echocardiograms of the tricuspid valve revealed diastolic doming in all patients with TS. Diastolic doming of the tricuspid valve was detected most often (all of 7 patients) in the apical 4-chamber view. In contrast, no patients without TS who had a decreased EF slope on the M-mode echocardiogram showed diastolic doming. These data suggest that a reduced DE amplitude of less than or equal to 10 mm associated with a decreased EF slope on the M-mode echocardiogram and diastolic doming of the tricuspid valve on the 2-D echocardiogram are useful echocardiographic signs in the diagnosis of TS.

Isolated rat heart preparations were used to determine the effect of cardioplegia on myocardial metabolism during profound hypothermic (15 degrees C) ischemia. The hearts were grouped according to the components of cardioplegia and the mode of administration. The six groups were normokalemic (GI), calcium-containing hyperkalemic (GII), calcium-free hyperkalemic (GIII) and single dose (A), multidose (B). Following 120 min of ischemia, tissue ATP decreased from 25.4 +/- 2.2 to 10.3 +/- 2.7, 3.9 +/- 2.4, 4.1 +/- 1.2, 15.5 +/- 3.2, 14.5 +/- 2.4 and 20.0 +/- 2.7 (I-A vs II-A p less than 0.005, I-A vs III-A p less than 0.005, I-B vs III-B p less than 0.05, II-B vs III-B p less than 0.005), and tissue lactate increased from 9.6 +/- 1.5 to 163.4 +/- 12.0, 174.1 +/- 13.5, 166.8 +/- 21.3, 99.1 +/- 8.3, 102.6 +/- 12.2 and 83.5 +/- 9.3 (I-B vs III-B p less than 0.02, II-B vs III-B p less than 0.02) mumol/dry wt g, in GI-A, GII-A, GIII-A, GI-B and GII-B, respectively. The results of this study suggests that (1) potassium cardioplegia in a single dose does not prevent degradation of high energy phosphate (HEP) in the hypothermic arrested heart, (2) though multidose cardioplegia is effective in preserving HEP during ischemia, the extent of its effects varies with the composition, and (3) the omission of calcium is beneficial in GIK cardioplegia in terms of preserving HEP at the end of ischemia.

A randomized, prospective study of the effectiveness of preoperative administration of coenzyme Q10 on the prophylaxis of postoperative low cardiac output state was performed in 50 patients with acquired valvular diseases necessitating valve replacement. There were 25 patients in the treatment group and 25 in the control group. Patients in the treatment group received 30 to 60 mg of coenzyme Q10 orally for six days before operation. Preoperative clinical variables, operative procedures, total cardiopulmonary bypass time, and aortic cross-clamping time were similar for the two groups. Postoperatively, mild to severe low cardiac output state developed in 28 of 50 patients (56%) and necessitated the administration of considerable amounts of inotropic agent. The treatment group showed a significantly lower incidence of low cardiac output state during the recovery period than the control group (p less than 0.05). These results suggest that preoperative administration of coenzyme Q10 will increase the tolerance of human hearts to ischemia during aortic cross-clamping.

Two solutions, our cardioplegic solution and Collins’ solution, were tested with regard to preservation of the heart under deep hypothermia before transplantation. The setup used was the isolated perfused working rat heart model and 4 hours of preservation at 0° C. The following three groups were prepared: Group 1: the heart was arrested with the cardioplegic solution (potassium: 20 mmol/L, sodium: 87 mmol/L) and then flushed with and stored in Collins’ solution (potassium: 117 mmol/L, sodium: 10 mmol/L); Group 2: the heart was arrested with and stored in Collins’ solution; and Group 3: the heart was arrested with and stored in the cardioplegic solution. The recovery of cardiac function was more satisfactory in Group 1 than in Groups 2 and 3. The increase in lactate was greater, and adenosine triphosphate and total adenine nucleotide were more depleted during storage in Group 2 than in Groups 1 and 3. In Group 3 myocardial sodium accumulation and potassium depletion during storage were greater than in Groups 1 and 2, and myocardial sodium and calcium overload after reperfusion were greater than in Group 1. Myocardial calcium overload after reperfusion in Group 2 was also greater than that in Group 1. These findings plus coronary vascular resistance analysis revealed that Collins’ solution damages the heart during arrest procedures and that the cardioplegic solution is less effective for storage of the arrested heart under deep hypothermia. Therefore the heart should be first arrested with the cardioplegic solution and then flushed with and kept in Collins’ solution for simple cold storage.

The protective effects of trimetazidine on postischemic cardiac function were studied using isolated working rat heart preparations in which global ischemia had been induced with normothermic cardioplegia. After 30 minutes of reperfusion, following a 25 minutes period of ischemia, the addition of 10(-6) M or 10(-5) M trimetazidine to the cardioplegic solution significantly increased the per cent recovery of the cardiac output: from 54.8 +/- 4.1 per cent in the control group to 81.0 +/- 3.2 per cent (p less than 0.01) and 79.6 +/- 4.0 per cent (p less than 0.01), respectively, although lower (10(-7) M) or higher (10(-4) M) doses of the drug failed to result in any change. 10(-5) M trimetazidine also produced a significantly greater recovery of both the postischemic aortic flow: from 47.8 +/- 4.9 per cent to 72.2 +/- 3.8 per cent (p less than 0.01) and coronary flow: from 80.6 +/- 2.9 per cent to 105.2 +/- 6.3 per cent (p less than 0.002). However, trimetazidine did not influence the recovery of either aortic pressure or heart rate. These results suggest that trimetazidine does give some protection to the heart during ischemia and reperfusion.

The effects of complete right bundle branch block (CRBBB) on the early postoperative course and long-term follow-up results of closure of ventricular septal defect (VSD) were investigated. (1) Postoperative change in cardiothoracic ratio (CTR): In patients whose ratio of total pulmonary resistance to total systemic resistance (Rp/Rs) was > 0.33, CTR of the group with CRBBB did not decrease significantly (p > 0.1) but CTR of the group without CRBBB was improved markedly (p

The influence of graded perfusion pressure (30, 60, and 90 mmHg) at cardiopulmonary bypass were studied on beating empty hearts (BEH) or spontaneously fibrillating hearts (SFH) in the normothermic state. The adequacy and distribution of coronary flow and the myocardial oxygen consumption (MVO2) were examined using the tracer microsphere technique in twelve mongrel dogs. In the SFH, the left ventricular (LV) endocardium (ENDO)/epicardium (EPI) flow ratio indicated significant decrease at 30 and 60 mmHg (0.83 +/- 0.05 and 0.86 +/- 0.06, p less than 0.005, respectively), but was recovered to control value at 90 mmHg (1.01 +/- 0.13). In the BEH, these low perfusion pressures did not result in an abnormal flow distribution in the LV (1.03 +/- 0.03 at 30 mmHg). The flow distribution to the right ventricle (RV) relatively increased in both the BEH and the SFH (p less than 0.001). The ENDO/EPI ratio of the RV did not decrease at 30 mmHg in both groups (1.11 +/- 0.03 in BEH and 1.16 +/- 0.08 in SFH). Coronary blood flow and MVO2 were significantly higher in the SFH than in the BEH. Coronary blood flow increased significantly with increase in the perfusion pressure, in both groups. The MVO2 was constant in the BEH, regardless of the perfusion pressure, but increased in the SFH at increasing pressure. These results show that in the SFH, subendocardial underperfusion of the LV is induced at the perfusion pressure of 30 and 60 mmHg.

Topical cardiac hypothermia is widely accepted and affords a measure of protection of the myocardium in cardiac surgery. As the most suitable temperature for such a preservation remains controversial, we prepared an animal model to carry out related experiments. An isolated working rat heart preparation was used to compare the hearts divided into three groups according to different temperatures during ischemia and reperfusion. During ischemia, the hearts in groups A and C were preserved at 5°C and the hearts in group B at 15°C. After one hour of ischemia, the hearts in groups A and B were reperfused at 27°C and rewarmed gradually to 34°C. The hearts in group C were reperfused at 20°C and rewarmed to 34°C. Following 50 min of reperfusion, cardiac output recovery was significantly better in group C, compared to group A (P < 0.02) and group B (P < 0.001). The hearts in group B released a significant large amount of lactate compared with the hearts in group A (P < 0.005) and group C (P < 0.001). The total amount of creatine phosphokinase (CPK) release during reperfusion was 1.14 ± 0.27 in group A, 1.26 + 0.22 in group B, and 0.49 ± 0.09 IU/heart in group C, respectively. These data show that (1) cold exposure at 5°C has no deleterious effect on myocardial function, (2) myocardial preservation at 5°C has more beneficial effects on depressing the myocardial metabolism than at 15°C, and (3) additional myocardial protection was obtained by lowering the perfusate temperature at the early reperfusion period.

A retrospective study of 21 adult patients with tetralogy of Fallot (TOF) was undertaken to determine the predisposing risk factors of renal dysfunction following total correction of the disease. Five of the 21 patients exhibited moderate-to-severe postoperative azotemia and an additional five exhibited mild azotemia. Significant risk factors for postoperative renal dysfunction found in routine preoperative examinations were as follows: arterial oxygen saturation of less than 90%, cardiothoracic ratio (CTR) of greater than 50%, mean electrical axis of the QRS complexes of greater than +120 degrees, S wave in Lead V6 of greater than 7 mm, R/S voltage ratio in Lead V6 of less than 2, and negative T wave in Lead V6. In addition, preoperative cardiac catheterization data showed that the patients exhibiting postoperative azotemia had more severe pulmonary stenosis, a smaller pulmonary-to-systemic flow ratio (Qp/Qs), and a larger left ventricular cavity than nonazotemic patients. The incidence of postoperative low cardiac output state (LOS) was significantly higher in the azotemic patients. These findings suggest that a combination of the severe form of TOF and a large left ventricle increase susceptibility to LOS and postoperative renal dysfunction. The cause and the clinical significance of the large left ventricular cavity in adults with TOF are discussed.

In 12 dogs being supported by cardiopulmonary bypass, the relationship among myocardial oxygen consumption and four energy-consuming factors (basal metabolism, heart rate, tension development, and external work) was studied. Tension (internal work) in the left ventricular wall was evaluated by myocardial tissue pressure with a Mikro-Tip pressure transducer. In an empty beating heart with constant perfusion pressure, both systolic tissue pressure and developed tissue pressure represented the same characteristics as developed tension measured by other methods. As the heart rate was increased, the systolic tissue pressure and developed tissue pressure continued to increase stepwise (Bowditch effect) up to some stimulation rate, at which, however, a decrease began despite a further increase in heart rate (Woodworth effect). Significant regression was established between myocardial oxygen consumption and heart rate, tension (developed tissue pressure x heart rate), and external work (minute work): myocardial oxygen consumption = (9.05 x 10(-3) heart rate) + (1.95 x 10(-4) developed tissue pressure) x heart rate + (1.63 x 10(-3) minute work) + 1.42 (r = 0.7999), where activation energy = 9.05 x 10(-3) ml/100 gm per beat, tension-related energy = 1.95 x 10(-4) ml/100 gm per unit of internal work, energy for work = 1.63 ml/100 gm per unit of external work, and basal metabolism = 1.42 ml/min/100 gm. We concluded that myocardial tissue pressure is a good substitute for tension and that multiple regression with heart rate, tension, and external work (as by modified Fenn's equation) seems indispensable to predict myocardial oxygen tension in the whole heart.

An isolated working rat heart preparation was used to determine the effect of diltiazem, a calcium antagonist, on the myocardial metabolism and functional recovery in the ischemic and reperfused heart, under conditions of 15 degrees C of topical hypothermia. The hearts were divided into two groups according to the solution injected into aortic root at the onset of ischemia. Group I (25 hearts) were given 3 ml of cold Krebs-Henseleit bicarbonate buffer solution (KHB), and Group II (25 hearts) were given the same dose of KHB containing 300 micrograms of diltiazem. After 30 min of reperfusion following 120 min of ischemia, cardiac output (ml/min) was significantly better in Group II (24.1 +/- 3.2) than in Group I (9.5 +/- 2.5). There were no differences between the groups with regard to tissue levels of creatine phosphate, adenosine triphosphate (ATP), total adenine nucleotide (TAN), glucose-6-phosphate and lactate during the ischemia. However, ATP and TAN levels were significantly higher in Group II after 30 min of reperfusion. These data show that, although diltiazem has little effect in preventing the catabolism of high-energy phosphates during hypothermic ischemia, there was an improvement in myocardial metabolism and an enhanced functional recovery during reperfusion in the diltiazem-treated hearts.

Aortocoronary bypass was performed on a patient with Takasyasu's arteritis whose first symptom of the disease was angina pectoris. The seriousness of the coronary arterial involvement in Takayasu's arteritis and the effectiveness of aortocoronary bypass should be given due consideration.