In-vitro effects of cardioplegic solutions on human saphenous vein endothelium--a scanning electron microscopy study.

In order to evaluate the effects of potassium cristalloid cardioplegic solutions (CPS) on the endothelial morphology, human saphenous veins were studied by scanning electron microscopy after exposure to three CPS named MKP (magnesium-potassium-procaine cardioplegia), LK (low-potassium cardioplegia), and HKA (high-potassium-albumin cardioplegia) and to their main components. Vein rings, selected from the saphenous veins sampled for graft harvesting in 63 patients undergoing aorto-coronary bypass surgery, were exposed for 30, 60, and 120 minutes to the following buffered solutions: Krebs bicarbonate (as control); MKP cardioplegia; KCl (16.0 mmol/L); MgCl2(2).6H2O (16.0 mmol/L); Procaine (0.05 mmol/L); NaCl (92.5 mmol/L); LK cardioplegia; KCl (10.0 mmol/L); Mannitol (74.3 mmol/L); Glucose (27.7 mmol/L); HKA cardioplegia; KCl (30 mmol/L). Severe endothelial lesions, consisting of diffuse disendothelialization and diffuse signs of endothelial suffering, were induced by KCl (30 and 16 mmol/L) after 60-120 min, and by MKP cardioplegia and KCl (10 mmol/L) after 120 min. Moderate endothelial lesions, characterised by diffuse endothelial surface changes and focal cellular loss, were induced by KCl (30 and 16 mmol/L) after 30 min, MKP cardioplegia and KCl (10 mmol) 30-60 min, LK cardioplegia, HKA cardioplegia, and MgCl2.6H2O after 120 min. Slight endothelial lesions, consisting of diffuse endothelial bulging, or absence of significant endothelial changes, were found in samples otherwise treated. Our findings showed a significant damaging effect of CPS on the human saphenous vein endothelium in-vitro. The endothelial lesions seemed related to the presence of potassium and magnesium, and to prolongation of the time of exposure to the cardioplegic solutions.(ABSTRACT TRUNCATED AT 250 WORDS)

Herpes simplex pneumonia in a heart transplant recipient.

An unusual case of Herpes simplex virus (HSV) pneumonia in a heart transplant recipient receiving chronic immunosuppressive therapy is reported. This infection presented an indolent course manifested by a chronic left pulmonary infiltrate unresponsive to antibiotic therapy and mild hypoxemia. Death eventually occurred as a consequence of an other infectious complication of the postoperative period. The HSV etiology of the necrotizing pneumonia observed at autopsy was established on the basis of histologic findings.

[Circadian rhythm of the renin-angiotensin-aldosterone system in subjects with kidney and heart transplants]. / Ritmo circadiano del sistema renina-angiotensina-aldosterone in soggetti con trapianto di rene e di cuore.

The present investigation evaluates the circadian rhythm of renin-angiotensin-aldosterone system (RAAS) in subjects with kidney (KTS) or heart (HTS) transplantation undergoing conventional therapy with prednisone and cyclosporine. RAAS circadian rhythmicity has been compared with the circadian cycle of cortisol as a marker rhythm. The chronobiological exploration has been performed by measuring the circulating levels of plasma renin activity (PRA), plasma aldosterone (PA), and serum angiotensin-converting-enzyme (SACE) and plasma cortisol (PC) in serial samplings collected six times over a 24-h span. Time-qualified levels of plasma cyclosporine (CYCL) have been established. The control group consisted of 10 normal subjects matching in age and sex. Individual data series were analysed by the Cosinor method. The chronobiometric estimates demonstrate the lack of a circadian rhythmicity for PRA, PA and SACE in KTS and HTS. The PC circadian rhythm is demonstrable in KTS, but not in HTS. The abolition of the RAAS circadian rhythm in both KTS and HTS seems to be attributable to the effects exerted by CYCL. The disappearance of the PC circadian rhythm may be due to the prednisone therapy that is administered twice a day in HTS but not in KTS. The asynchronous effects of this drug lead us to suggest that antirejection therapy may be optimized by administering prednisone and cyclosporine according to a chronomodulated scheme.

The role of indium-111 antimyosin (Fab) imaging as a noninvasive surveillance method of human heart transplant rejection.

The identification of rejection after heart transplantation in patients receiving cyclosporine immunosuppressive therapy requires the endomyocardial biopsy, an invasive method associated with a finite morbidity. To evaluate the role of indium-111 antimyosin (Fab) scintigraphy as a noninvasive surveillance method of heart transplant rejection, the Fab fragment of murine monoclonal antimyosin antibodies labeled with indium-111 was administered intravenously in 30 scintigraphic studies to 10 consecutive heart transplant recipients. Endomyocardial biopsy specimens were obtained 72 hours after each scintigraphic study. Nineteen scintigraphic studies had negative findings; no false negative finding was obtained. Eleven antimyosin scintigraphic studies had positive findings, and in these studies endomyocardial biopsy revealed mild rejection in two cases, moderate acute rejection with myocyte necrosis in two cases, myocyte necrosis as a consequence of ischemic injury in six cases, and possibly cytotoxic damage in one case. Antimyosin scintigraphy may represent a reliable screening method for the surveillance of heart transplant patients. In the presence of a negative finding from antimyosin scintigraphy, it may be possible to avoid endomyocardial biopsy. Conversely, in patients who have a positive finding from antimyosin scintigraphy, the endomyocardial biopsy is mandatory to establish the definitive diagnosis by histologic examination of the myocardium.

Ultrastructural changes of coronary artery endothelium induced by cardioplegic solutions.

Coronary artery endothelial and myocardial ultrastructure was studied in guinea-pig heart-lung preparations (HLP) subjected to ischemic cardiac arrest induced by three hypothermic solutions. Two of the solutions used had high potassium chloride concentration ("Alabama" and "St. Thomas") while the third, instead, was a bicarbonate buffer (Kreb's solution). Five experimental groups were studied. In group 1 (control) the HLP were not subjected to cardiac arrest. Groups 2, 3, and 4 were subjected to a period of cardiac arrest of 30, 60, and 120 minutes respectively. In group 5, HLP were reperfused with blood for 30 minutes after 60 minutes of cardiac arrest. A thin ring of the left anterior descending coronary artery and myocardial fragments were obtained at the end of each experiment and were analyzed by means of transmission electron microscopy (TEM). Functional parameters were recorded in group 5. HLP perfused with Alabama solution showed a well-preserved endothelium and myocardium. HLP perfused with Krebs solution showed slight changes of the endothelial glycocalix only in group 4. Further, HLP perfused with Krebs solution showed extensive myocardial lesions (groups 3 and 4). These ischemic changes were not completely reversed after reperfusion (group 5). HLP perfused with St. Thomas solution showed only endothelial changes. These lesions were mainly characterized by: disappearance of the glycocalix and pynocytotic vesicles, endothelial cell bulging (group 2), and loss of the endothelial continuity (groups 3, 4, and 5). Hemodynamic parameters were significantly changed only in the Krebs-perfused HLP which showed a deterioration of the cardiac function related to the ischemic damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium entry blockers and cardioplegia: interaction between nifedipine, potassium, and hypothermia.

The potential additive protective effect provided by nifedipine to the University of Alabama Hospitals cardioplegia solution (ACS) was assessed with the use of a guinea pig heart-lung model of cardiopulmonary bypass and ischemic arrest. The addition of nifedipine consistently enhanced the protective properties of ACS infused at 37 degrees C; functional recovery was similar to that observed with cold ACS. Despite the additional protection under normothermic conditions, nifedipine did not improve recovery after infusion at 4 degrees C. The abolition by hypothermia of the protective effects of nifedipine suggests a similarity in action between nifedipine and hypothermic protection. The interaction between ACS and nifedipine was studied on bovine coronary arteries in vitro. Nifedipine caused a marked reduction in the coronary vasoconstricting effect of ACS, both under normothermic and hypothermic conditions. The use of nifedipine in cardioplegia may provide additional protection when uneven distribution of the cardioplegic solution is expected and hypothermic protection is unreliable.

[Effects of cardioplegic solutions on coronary and myocardial ultrastructure. Preliminary note]. / Effetti delle soluzioni cardioplegiche sull'ultrastruttura coronarica e miocardica. Nota preliminare.

Ultrastructural changes of the myocardium and the coronary arterial endothelium were studied following cold perfusion with two different cardioplegic solutions (CPS) (the University of Alabama and the St. Thomas Hospital solutions), and with Krebs' solution as a control (CS). Guinea pig heart-lung preparations (HLP) were subjected to cardiac arrest by perfusion under CPS or CS (4 ml/Kg/min. X 4 min.). The duration of the cardiac arrest was 60 minutes, and additional amounts of cold solution were perfused after the first 30 minutes. In a second experimental group, HLP were reperfused with blood following 60 minutes of cardioplegic arrest, and maintained under full activity for the next 30 minutes. At the end of the study, specimens of coronary artery and myocardium were obtained and observed by Scanning (SEM) and Trasmission (TEM) electron microscopy. All the specimens were compared with additional specimens obtained from control hearts not subjected to cardiac arrest. The myocardial ultrastructure of hearts arrested with CPS was well preserved, whereas severe myocardial damage, consisting in the absence of glycogen granules, intracellular edema and myofibrillar contraction, was following CS-induced cardiac arrest. In contrast, perfusion with the St. Thomas CPS produced severe vascular damage, characterized by interruption of the endothelial layer, and bulging of endothelial cells into the lumen; no vascular changes were observed following cardiac arrest with CS or Alabama CPS. We conclude that the damage to the coronary arterial endothelium is not related to cardiac arrest, or to perfusion with cristalloid solution, or to myocardial damage, but appears to depend on the composition of the CPS.

Management of massive air embolism during open-heart surgery with retrograde perfusion of the cerebral vessels and hyperbaric oxygenation.

Retrograde perfusion through the superior vena cava was used in 2 patients who were injured by massive air embolism occurring during open-heart surgery. They underwent hyperbaric treatment immediately following completion of the intracardiac repair. Both patients made complete recovery and were discharged, with no defects attributable to the incident.

[Value of a rational postoperative treatment protocol in cardiac surgery]. / L'importanza del protocollo di trattamento postoperatorio nella chirurgia cardiaca.

The postoperative course of 76 patients, who underwent valve and/or coronary surgery during a period of 18 months, was analyzed to determine the influence of the overall non-surgical management on the results of the operations. We used an approach (System analysis) based upon analysis of the cardiac, pulmonary, renal, general metabolic, neurologic, and gastrointestinal subsystems. The use of inotropic support and the incidence of postoperative arrhythmias were lower. The permanence in intensive care unit and the hospital postoperative course were shorter in comparison with all series of patients who had the same type of surgery over the same period in our unit. These results indicate that the postoperative care after cardiac surgery needs accurate analysis, precise deductions and effective treatment.