Myocardial neutrophil sequestration during reperfusion of the transplanted rabbit heart.

BACKGROUND: Neutrophils are major participants in myocardial reperfusion injury, but the relationship between ischemic time and the extent of the neutrophil sequestration in heart transplantation has not yet been systematically studied. This study was designed to determine whether increased ischemic time would cause greater neutrophil sequestration during reperfusion of the globally ischemic heart. METHODS: Rabbit hearts were arrested with cardioplegia, explanted, and subjected to either 1 or 4 hours of global ischemia at 4 degrees C before being heterotopically transplanted into a recipient rabbit's abdomen for reperfusion. Each heart was reperfused for either 4, 8, or 12 hours. Between 3 and 7 hearts were studied (average = 5.8) for each combination of ischemic and reperfusion time (total = 35). A myeloperoxidase (MPO) assay was used to qualify neutrophil content. RESULTS: MPO activity (U/g wet weight) was not significantly different at 4, 8, and 12 hours of reperfusion (0.33 +/- 0.05, 0.20 +/- 0.04, 0.26 +/- 0.04: p = 0.13), but was significantly increased at 4 hours compared to 1 hour ischemia (0.34 +/- 0.04 vs 0.19 +/- 0.03: p = 0. 006). Interaction between ischemic and reperfusion times was not significant (p = 0.12). MPO activity was below the measurable threshold in 5 freshly excised control hearts. CONCLUSIONS: These results suggest that acute reperfusion injury will be more severe in the hearts subjected to 4 hours ischemia and indicate the need to consider neutrophil-mediated reperfusion injury when addressing cardioprotective interventions for cardiac preservation and reperfusion after transplantation. Neutrophil-mediated reperfusion injury of the rabbit myocardium after heterotopical transplantation is more severe in hearts subjected to 4 hours of ischemia vs 1 hour of ischemia prior to transplantation.     

NOS substrate during cardioplegic arrest and cold storage decreases stunning after heart transplantation in a rat model.

BACKGROUND: In this study, we evaluated how adding L-arginine to Centre de Résonance Magnétique Biologique et Médicale (CRMBM) solution affected myocardial performance during post-ischemic in vivo reperfusion. METHODS: Experiments were conducted using a modified Lewis-Lewis heterotopic heart transplantation model, with a total ischemic time of 3 hours followed by 1 or 24 hours of blood reperfusion. Heart grafts were arrested using intra-aortic injection of CRMBM solution, either supplemented or not supplemented with 2 mmol/liter L-arginine (n = 12 in each group). We measured systolic indexes and simultaneously performed phosphorus magnetic resonance spectroscopy ((31)P MRS). We quantified total endothelial nitric oxide synthase (eNOS) protein using the Western blot test of freeze-clamped hearts. RESULTS: Contractility during early reperfusion was significantly better in grafts arrested with CRMBM solution enriched with L-arginine: mean rate pressure product, 11249 +/- 1548 vs 5637 +/- 1118 mm Hg/min (p = 0.05), and maximal first derivative of the pressure signal (dP/dt(max)), 1721 +/- 177 vs 1214 +/- 321 mm Hg/sec (p = 0.013). Conversely, during late reperfusion, contractility did not relate to the nature of the preservation solution. The presence of L-arginine in the CRMBM solution did not alter time-related variations of high-energy phosphate ratios measured using in vivo (31)P MRS. The eNOS protein level decreased significantly during early compared with late reperfusion, with no effect caused by L-arginine. CONCLUSIONS: During early reperfusion, the limited myocardial stunning observed with CRMBM solution containing L-arginine does not relate to energy metabolism but to better preservation of the NO pathway.     

Effects of inosine on reperfusion injury after heart transplantation.

OBJECTIVE: Inosine, a break-down product of adenosine, has been recently shown to exert inodilatory and anti-inflammatory properties. We investigated the effects of inosine on ischemia/reperfusion injury in a rat heart transplantation model. METHODS: Intraabdominal heterotopic transplantation was performed in Lewis rats. After 1h of ischemic preservation, reperfusion was started after application of either saline vehicle (control, n=12) or inosine (100 mg/kg, n=12). Coronary blood flow, left ventricular function, endothelium-dependent vasodilatation to acetylcholine and endothelium-independent vasodilatation to sodium nitroprusside, and high energy phosphate content were measured after 1 and 24h of reperfusion. In addition, the activation of the poly(ADP-ribose) polymerase was detected by immunhistology. RESULTS: After 1h, coronary blood flow (4.1+/-0.3 ml/(ming) vs 2.9+/-0.3 ml/(ming), p<0.05), left ventricular systolic pressure (102+/-9 mmHg vs 83+/-4 mmHg, p<0.05) and dP/dt (2765+/-609 mmHg/s vs 1740+/-116 mmHg/s, p<0.05) were significantly higher in the inosine group in comparison to control. Vasodilatatory response to sodium nitroprusside was similar in both groups. Acetylcholine resulted in a significantly higher increase in coronary blood flow in the inosine group (76+/-5% vs 48+/-9%, p<0.05). Energy charge potential was significantly higher in the inosine group (1.69+/-0.10 micromol/g vs 0.74+/-0.27 micromol/g, p<0.05). After 24h, there was no difference between the groups in basal coronary blood flow, left ventricular systolic pressure, dP/dt, and the response to sodium nitroprusside. However, acetylcholine led to a still significantly higher response in the inosine group (112+/-13% vs 88+/-7%, p<0.05). Immunhistologic stainings revealed activation of poly(ADP-ribose) polymerase in control animals which was abolished by inosine. CONCLUSIONS: Thus, inosine improves myocardial and endothelial function during early reperfusion after heart transplantation with a persisting beneficial effect against reperfusion induced graft coronary endothelial dysfunction. The effects of inosine are mediated at least partly by modulation of the peroxynitrite-poly(ADP-ribose) polymerase pathway.     

Differential expression of neutrophil adhesion molecules during coronary artery surgery with cardiopulmonary bypass.

BACKGROUND: Activation of neutrophil adhesion molecules and subsequent neutrophil adhesion to vascular endothelium are key events initiating inflammatory organ dysfunction after cardiopulmonary bypass and ischemic reperfusion. OBJECTIVES: We sought to characterize neutrophil integrin CD11b and L-selectin activation associated with coronary artery bypass graft surgery and to determine whether neutrophil activation contributes to their sequestration on postbypass reperfusion. METHODS: Twenty patients undergoing routine coronary artery bypass were studied. Heparinized whole blood was simultaneously sampled from a central venous line, aorta, coronary sinus, and right and left atrium before, during, and up to 20 minutes after cardiopulmonary bypass. Neutrophil counts were obtained, and neutrophil CD11b and L-selectin expression was determined by flow cytometric analysis in whole blood. RESULTS: CD11b expression on circulating neutrophils increased during cardiopulmonary bypass, peaking at 145% of baseline level after release of the aortic clamp and then declined by 20 minutes after bypass (analysis of variance, P =.003). No change in neutrophil L-selectin expression was observed during cardiopulmonary bypass. Neutrophils responded to ex vivo stimulation by C5a and leukotriene B(4) during cardiopulmonary bypass but not at 24 hours after the operation. After reperfusion, neutrophil loss, but not local activation, was demonstrated in the coronary and pulmonary circulations. CONCLUSIONS: Upregulated CD11b expression on neutrophils is likely to contribute to neutrophil sequestration in the heart and lungs after bypass, but neutrophil activation may be limited by their reduced responsiveness to agonist stimulation. CD11b represents a potential therapeutic target for diminishing inflammation after cardiac operations.     

Relation between long-term steroid treatment after heart transplantation, hypofibrinolysis and myocardial microthrombi generation.

BACKGROUND: Thrombotic complications and transplant coronary artery disease are among the main causes of morbidity and mortality after heart transplantation. A thrombophilic state has been described in transplant recipients, and correlated to immunosuppressive therapy with cyclosporine A or azathioprine, whereas the prothrombotic effects of steroids, even though always given, have never been duly considered. A reduced fibrinolytic capacity due to high levels of PAI-1, the most important inhibitor of plasminogen activators, was suggested to play a role in the development of cardiovascular diseases and transplant coronary artery disease. A severe hypofibrinolytic state secondary to PAI-1 increase has been found in patients with Cushing's disease, and in hypercorticism secondary to long-term steroid treatment after renal transplantation. METHODS: We evaluated plasma clotting and fibrinolytic behaviors in 2 groups of heart transplant patients treated with (26 cases) or without (23 cases) steroids together with cyclosporine A and azathioprine. Twenty-five healthy subjects were studied as normal controls. The following tests were assayed at least 1 year after transplantation: fibrinogen, factor VIII coagulant activity, von Willebrand factor antigen, euglobulin lysis time, tissue plasminogen activator antigen and activity, PAI-1 antigen and activity. In addition, the presence of cardiac microthrombi was evaluated on 2 endomyocardial biopsy specimens obtained in each patient both on day 7 after heart transplantation (first control) and usually 1 year or more later (last control). RESULTS: Plasma levels of fibrinogen, factor VIII and von Willebrand factor were significantly higher in both groups of patients than in normal controls. Fibrinolytic activity was significantly reduced in transplant patients treated with steroids, compared with steroid-free patients and normal controls. In steroid-treated heart transplant recipients, the hypofibrinolytic state was due to a significant and pathological increase in PAI-1 antigen and activity levels. The fibrinolytic impairment was more evident in patients transplanted for ischemic heart disease and treated with steroids than in patients with previous dilated cardiomyopathy and treated either with or without steroids. Myocardial microthrombi were found in 2/49 cases at the first biopsy control, and in 12/49 cases at the last biopsy control after transplantation. This different prevalence was statistically significant (chi2 = 8.33, p = .003). Plasma PAI-1 activity was significantly higher and, as a consequence, euglobulin lysis time was more prolonged in microthrombi-positive patients than in microthrombi-negative ones. Among the 12 transplant recipients who developed cardiac microthrombi, 7 patients were treated with steroids and showed higher PAI-1 levels and more reduced fibrinolytic activity than the 5 steroid-free patients. CONCLUSIONS: Our data confirm the prothrombotic state induced by long-term steroid treatment, characterized by an increase in PAI-1 levels and secondary impairment of fibrinolytic capacity. In heart transplant patients, steroid-related hypofibrinolysis might constitute a further risk factor for transplant coronary artery disease.     

Myocardial protection by blood cardioplegia and warm reperfusion in heart transplantation.

We describe the technique of blood cardioplegia delivery as we routinely use it in clinical heart transplantation. This technique needs a specific circuit. Perfusion of a first dose of blood cardioplegia is immediately started on the arrival of the graft in the operating room. Cardiac reperfusion of a half-dose of blood solution without potassium is performed each 20 minutes. Myocardial warm reperfusion is started at the end of the aortic suture. This technique of blood cardioplegia and warm reperfusion during heart transplantation provided an improvement in heart preservation when compared with standard crystalloid solution.     

再灌注期低体温对慢性重型肝炎患者肝移植术后急性肺水肿的影响

目的 探讨再灌注期低中心体温对慢性重型肝炎患者肝移植术后急性肺水肿(APE)的影响.方法 回顾性分析2002年2月至2006年12月间诊治的108例慢件重型肝炎肝移植患者的临床资料.比较肝移植术后急性肺水肿(APE组)和无急性肺水肿(NAPE组)患者再灌注期低体温持续时间,及其对输血量和新肝期凝血酶原时间(PT)的影响.结果 108例患者中有41例在肝移植术后发生不同程度的APE(37.96%).APE组患者再灌注期体温比NAPE组更低(t=2.413,P=0,018),低体温持续时间超过5 min的病例数更多(39.02%,x2=143.40).APE组患者新肝期PT延长更加明显(t=2.884,P=0.005),输血量更大.低体温组患者与对照组比较,新肝期PT更长[分别为(28.03±8.45)min和(24.12±5.89)min,t=2.553,P=0.012],输注的红细胞量[分别为(2786.96±1266.47)ml和(2129.4.1±805.90)ml,t=2.364,P=0.026)和血浆量均更多[分别为(2121.74±676.19)m1和(1768.24±685.08)ml,t=2.201,P=0.030].结论 再灌注期中心体温过低增加慢性重型肝炎肝移植术后急性肺水肿的发生率,可能与凝血酶原时间延长、增加输血最有关.     

心脏移植受者术后感染特点及防治策略

目的 探讨心脏移植受者术后感染的特点及相应的防治策略.方法 回顾性研究规律随访的140例心脏移植受者的病史资料.术后患者均接受抗细菌感染的预防性治疗,其中87.8%的患者术后以抗病毒药物预防巨细胞病毒感染.患者的免疫抑制方案为他克莫司或环孢素A+吗替麦考酚酯+糖皮质激素.术后患者行咽拭子、痰涂片革兰染色、痰培养、血培养、尿培养和粪培养进行微生物监测,统计感染时间及病原体等资料.结果 心脏移植受者感染发生率为42.9%(60/140),随访期间共发生感染84例次,64例次(76.2%)发生在术后第1个月内,均治愈;20例次(23.8%)发生于2个月以后,其中4例患者死亡.结论 心脏移植受者术后早期细菌感染多见,预后佳;术后晚期真菌和病毒感染占较大比例,预后差.     

Valacyclovir prevention of cytomegalovirus reactivation after heart transplantation: a randomized trial.

BACKGROUND: Cytomegalovirus (CMV) is a major cause of serious morbidity following solid organ transplantation via both direct and indirect mechanisms. The aim of this study was to investigate the efficacy and safety of valacyclovir prophylaxis in heart transplant recipients. METHODS:Twenty-seven CMV seropositive adults due to receive a heart transplant were included in a single-center, randomized, double-blind study. Patients were randomized to receive either oral valacyclovir 2000 mg or oral acyclovir 200 mg four times daily starting within 3 days of heart transplant and continuing for 90 days. The primary outcome measure was time to development of CMV antigenemia assessed for 6 months after surgery. Other measures were time to asymptomatic CMV infection, symptomatic CMV infections, and end-organ CMV disease. Patients were monitored for other herpes infections, other opportunistic infections, and acute graft rejection. Safety was assessed by evaluating changes in hematology and clinical chemistry parameters and by the occurrence of adverse events. RESULTS: The median time to CMV antigenemia was 19 days for the acyclovir group compared with 119 days for the valacyclovir group (hazard ratio 0.42; 95% CI, 0.18-0.99; p = 0.049). Similar delays of approximately 100 days were found for CMV infection, symptomatic CMV infection, and CMV disease. There was also a trend for delayed acute rejection, and fewer opportunistic or other herpesvirus infections occurred in the valacyclovir group. Valacyclovir was well tolerated in the study population. CONCLUSION: Oral valacyclovir is a safe and effective mode of prophylaxis of CMV after heart transplantation.     

Capillary endothelia and cardiomyocytes differ in vulnerability to ischemia/reperfusion during clinical heart transplantation.

OBJECTIVE: The development of accelerated graft arteriosclerosis is a major cause of late death after orthotopic heart transplantation. The influence and the extent of peritransplant injury, especially of cardiomyocyte or capillary endothelial cell edema is discussed. METHODS: A morphometric ultrastructural analysis of myocardial biopsies from 29 donor hearts (21 male, age 34+/-11 years) was performed. Right ventricular biopsies were obtained before cardioplegia (A), immediately following cardioplegia (B) (Custodiol, Dr. F. K?hler Chemie GmbH, Alsbach-H?hnlein, Germany), before implantation (C), after 30 (D) or 60 (E) min of reperfusion and 1 week after transplantation (F). Mean ischemic time was 185+/-68 min. Quantitative electron microscopy was carried out in five samples per heart and time point and in 30 test fields per sample by 'random systematic sampling' and 'point and intersection counting'. As parameters for cell edema the volume density of myofibrils in cardiomyocytes and the mean barrier thickness of capillary endothelia were analyzed. P-values of less than 0.05 were regarded as significant. Significant differences in contrast to the previous values are marked by *. RESULTS: The volume density of myofibrils (vol.%) was as follows: (B) 63.6+/-3.2, (C) 61.8+/-3.2, (D) 62.9+/-3.2, (E) 63.6+/-4.5. The mean barrier thickness (nm) was as follows: (A) 353+/-21, (B) 376+/-59, (C) 416+/-71*, (D) 473+/-45*; (E) 453+/-50*, (F) 379+/-39. CONCLUSIONS: Apart from a generally accepted edema of cardiomyocytes a relevant capillary endothelial cell edema develops during clinical heart transplantation. In contrast to cardiomyocytes the cell edema of endothelia shows a more pronounced and significant progression during cold ischemia and early reperfusion. After 60 min of reperfusion it is still significantly more pronounced than at the onset of ischemia. After 1 week there are no statistical differences compared to the initial values. Thus, an edema of capillary endothelia probably will trigger inhomogeneities in capillary perfusion. Peritransplant injury of endothelia may contribute to the later development of accelerated allograft arteriosclerosis.     

Inhibition by dipyridamole of neutrophil adhesion to vascular endothelium during coronary bypass surgery.

BACKGROUND: Release of reactive oxygen radicals by activated neutrophils and neutrophil adhesion to endothelial cells have been observed after cardiopulmonary bypass. The aim of the present study was to evaluate the effects of preoperative dipyridamole treatment on neutrophil superoxide anion generation and endothelial cell-neutrophil interactions. METHODS: Two groups of patients scheduled for elective coronary artery bypass grafting were randomized to receive oral dipyridamole or a placebo. Nitro blue tetrazolium scores of circulating neutrophils, neutrophil CD11b/CD18 expression, and their adhesion to human umbilical vein endothelial cells were assayed before anesthesia, 30 minutes after the beginning of cardiopulmonary bypass, at the end of bypass, and 60 minutes postoperatively. RESULTS: In both groups, cardiopulmonary bypass resulted in a significant increase in nitro blue tetrazolium scores in circulating neutrophils as well as a significant increase in both neutrophil CD11b/CD18 expression and neutrophil adhesion to endothelial cells. The extent of neutrophil superoxide anion generation was higher in the control group; a significant (p < 0.01) reduction in neutrophil adhesion to endothelial cells was observed 1 hour postoperatively in the dipyridamole group. In 5 patients treated with dipyridamole, the incubation of activated polymorphonuclear leukocytes with adenosine deaminase significantly increased their adhesion to endothelial cells (p < 0.05). CONCLUSIONS: Our study demonstrated that preoperative treatment with oral dipyridamole significantly reduces both neutrophil superoxide anion generation and extent of neutrophil adhesion to endothelial cells after coronary bypass grafting procedures with cardiopulmonary bypass. The mechanism is probably mediated by endogenous adenosine.     

The effect of lidocaine on in vitro neutrophil and endothelial adhesion molecule expression induced by plasma obtained during tourniquet-induced ischaemia and reperfusion

BACKGROUND: Changes in neutrophil and endothelial adhesion molecule expression occur during perioperative ischaemia and reperfusion (I/R) injury. We investigated the effects of lidocaine on neutrophil-independent changes in neutrophil and endothelial adhesion molecule expression associated with tourniquet-induced I/R. METHODS: Plasma was obtained from venous blood samples (tourniquet arm) taken before (baseline), during, 15 min, 2 and 24 h following tourniquet release in seven patients undergoing elective upper limb surgery with tourniquet application. Isolated neutrophils from healthy volunteers (n = 7) were pretreated in the presence or absence of lidocaine (0.005, 0.05 and 0.5 mg mL(-1) for 1 h, and then incubated with I/R plasma for 2 h. Human umbilical vein endothelial cells (HUVECs) were pretreated in the presence or absence of lidocaine (0.005, 0.05 and 0.5 mg mL(-1)) for 1 h, and then incubated with the plasma for 4 h. Adhesion molecule expression was estimated using flow cytometry. Data were analysed using ANOVA and post hoc Student-Newman-Keuls tests. RESULTS: I/R plasma (withdrawn 15 min following tourniquet release) increased isolated neutrophil CD11b (P = 0.03), CD18 (P = 0.01) and endothelial intercellular adhesion molecule-1 (ICAM-1) (P = 0.008) expression compared to baseline. CD11b, CD18 and ICAM-1 expression on lidocaine (0.005 mg mL(-1)) treated neutrophils was similar to control. CD11b (P < 0.001), CD18 (P = 0.03) and ICAM-1 (P = 0.002) expression on lidocaine (0.05 mg mL(-1)) treated neutrophils and HUVECs was less than that on controls. CONCLUSION: Increased in vitro neutrophil and endothelial cell adhesion molecule expression on exposure to plasma obtained during the early reperfusion phase is diminished by lidocaine at greater than clinically relevant plasma concentrations.     

Severe diverticulitis after heart, lung, and heart-lung transplantation.

BACKGROUND: In this study, we reviewed our experience with severe diverticulitis in patients who have undergone heart and/or lung transplantation to assess whether transplant recipients are at increased risk of having severe diverticulitis compared with the general population. METHODS: We reviewed the records of patients who underwent heart and/or lung transplantation from 1984 to 2000, inclusive, and identified patients with severe diverticulitis that required surgery or that resulted in death. We compared this incidence with the incidence of such complications in the general population, served by the same institution during a 2-year period, 1999 to 2000. RESULTS: A total of 953 patients underwent transplantation in the study period. The mean follow-up was 57 months, a total follow-up of 4528 patient-years. Nine patients (mean age, 54 years) had severe diverticulitis that required surgical intervention (8 patients) or that resulted in death (1 patient died without surgical intervention). During 1999 to 2000, 16 patients (mean age, 66 years) from the general population were treated for severe diverticulitis that required surgical intervention, 3 of whom died. From census and area health data, we found that the study institution serves approximately 90000 people older than 40 years, with a total follow-up of 180000 patient-years. The incidence rate ratio for severe diverticulitis when comparing the transplant with the non-transplant groups was 22.2 (95% confidence interval; 9.9-50.0; p < 0.001). CONCLUSIONS: Patients with severe diverticulitis who have undergone heart and/or lung transplantation can be treated surgically with a small mortality rate. Transplant recipients probably are at substantially increased risk of experiencing severe diverticulitis.     

Development of myocardial beta-adrenergic receptor density and adenylate cyclase activity after human heart transplantation.

An increase in basal heart rate caused by a lack of vagal control and chronotropic supersensitivity to epinephrine has been shown in transplanted human hearts. Prejunctional and/or postjunctional origins for this supersensitivity have been suggested, the latter involving changes in the number of myocardial beta-adrenergic receptors or in the receptor adenylate cyclase system. To directly determine the time course of change, serial determinations were performed during the first 3 months after heart transplantation. The beta-adrenergic receptor density measured by iodine 125-labelled iodocyanopindolol binding in 61 endomyocardial biopsy specimens (a mean of 6.1 +/- 0.58 biopsies from each of 10 patients) showed great intraindividual and interindividual variability (56.6 +/- 6.8 fmol/mg protein) with no mean trend toward gradually changing receptor densities. Isoproterenol-stimulated adenylate cyclase activity measured in 33 biopsy specimens (a mean of 5.5 +/- 0.67 biopsy specimens from each of six patients) varied considerably (112.5 +/- 13.8 pmol cyclic adenosine monophosphate/mg protein/min), again with no definite tendency with regard to the development over time. The beta-adrenergic receptor densities showed no statistical correlation with the degree of rejection as assessed by histologic criteria and antimyosin ration. These results suggest that in the first 3 months after heart transplantation beta-adrenergic receptor density and adenylate cyclase responses to 10 mumol/L isoproterenol do not change and that beta-adrenergic receptor density in the transplanted myocardium does not seem to be affected by the degree of rejection.     

Sympathetic reinnervation after heart transplantation, assessed by iodine-123 metaiodobenzylguanidine imaging, and heart rate variability.

OBJECTIVE: Complete allograft denervation occurs during heart transplantation. Partial ventricular sympathetic reinnervation may develop one year or later after transplantation and can be measured with iodine-123-meta-iodobenziylguanidine (MIBG) uptake. Aim of this study was to assess sinus node sympathetic reinnervation measured with heart rate variability and ventricular sympathetic reinnervation evaluated with MIBG. METHODS: Twelve patients and 14 healthy controls were included. In patients, MIBG scintigraphy with early and late imaging was performed. Heart to mediastinum ratio (HMR) was calculated and patients were divided in groups with (HMR>1.3) and without left ventricular reinnervation (HMR<1.3). Bipolar ECG with high sampling rate and resolution was recorded over 8.5 min in supine position and in upright position after 10 min interval. R-R intervals in time domain and heart rate variability in frequency domain through spectral power analysis of R-R intervals were analysed to evaluate sinus node reinnervation. Spectral power in low frequency range (0.04-0.15 Hz) above 4.5 ms(2) was considered as sinus node sympathetic reinnervation. RESULTS: Six (50%) patients had evidence of left ventricular sympathetic reinnervation on scintigraphy. Sinus node sympathetic reinnervation based on heart rate variability was detected in 6 (50%) patients in supine, and in 4 (33%) patients in upright body position. Four patients groups were discerned: (1) with ventricular and sinus node sympathetic reinnervation, (2) with sinus node sympathetic reinnervation, (3) with ventricular sympathetic reinnervation and (4) without atrial or ventricular sympathetic reinnervation. Ventricular reinnervation process was time dependent and sinus node reinnervation was not. CONCLUSIONS: Simultaneous ventricular sympathetic reinnervation assessed by MIBG and sinus node sympathetic reinnervation assessed by heart rate variability in supine as in upright position were detected only in two patients (17%). The results of our study show that eventual sinus node sympathetic reinnervation and left ventricular sympathetic reinnervation do not occur simultaneously.     

Association of parvovirus B19 with plasma cell-rich myocardial infiltrates after heart transplantation.

In this report we describe the development of plasma cell-rich myocardial infiltrates in association with a parvovirus B19 infection in a heart transplant patient. We hypothesize that the virus, either alone or in association with the cardiac allograft, may polarize the immune response in the direction of T helper 2 (Th2) cells rather than the expected Th1 cells. This favors the development of a humoral immune response and infiltration of the graft with plasma cells.     

Use of cytochrome C in the prevention of myocardial reperfusion injury during heart valve prosthesis implantation under conditions of extracorporeal circulation

Cytochrome C used at the postischemic period causes a rapid reestablishment of coronary circulation, hemodynamic parameters, prevents activation of lipid peroxidation in reoxygenation of the heart after prolonged total myocardial ischemia in patients with acute bacterial endocarditis in whom the prostheses of heart valves had been fulfilled. Parallel with the positive inotropic effect, Cytochrome C reduces the postloading and, as a result, transfers the cardiac muscle to a more profitable regimen. At the end of the myocardial ischemia period Cytochrome C provides rapid and effective recovery of the bioelectrical function of the heart, improves its pumping function, thus allowing the dose and duration of inotropic stimulation of the myocardium at the postischemic period to be reduced, lowers pulmonary resistance and finally leads to less postoperative intrahospital lethality from acute heart failure.     

Protection by coenzyme Q10 of canine myocardial reperfusion injury after preservation.

This study was undertaken to assess whether pretreatment of the donor heart with coenzyme Q10 could improve postischemic myocardial recovery. Coenzyme Q10 or its solvent was administered intravenously to donor dogs 1 hour before isolation of the heart. Each heart was stored in Euro-Collins solution at 4 degrees C for 6 or 24 hours and then was reperfused via the aorta with arterial blood of a supporting dog for 3 hours at 37 degrees C in a working mode. During preservation, adenosine triphosphate level was significantly reduced in the placebo group from 21.0 mumol/gm dry weight to 15.1 and 11.9 after 6 and 24 hours of preservation, respectively. Coenzyme Q10 pretreatment maintained the adenosine triphosphate level at 18.9 even after 24 hours of preservation. After reperfusion following 6 and 24 hours of preservation, the adenosine triphosphate level recovered to the original level in the coenzyme Q10 group, but it remained significantly low in the placebo group. Preservation and subsequent reperfusion caused a significant increase in the level of malondialdehyde of hearts in the placebo group, and coenzyme Q10 pretreatment completely suppressed the increase in the malondialdehyde level after reperfusion. Ventricular functions were improved in the coenzyme Q10 group. These results support the concept that free radicals play an important role in myocardial injury during preservation and subsequent reperfusion and suggest that pretreatment of the heart with coenzyme Q10 is effective in preventing such injury that may develop after reperfusion.     

Complete transection of the median and radial nerves during arthroscopic release of post-traumatic elbow contracture.

Arthroscopic debridement and capsular release was performed in a 57-year-old woman because of post-traumatic stiffness in the dominant right elbow joint. During this procedure, the median and radial nerves were completely transected. A few recent reports of small series have described encouraging results after arthroscopic capsular release of post-traumatic elbow contracture, but the present case demonstrates the inherent risk of damage to neurovascular structures.