[Heart surgery in Sweden is sufficiently developed. Risk of expensive overuse].
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Biomedical subjects
Publications and source records attributed to K Rådegran.
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A patient underwent pulmonary thromboendoarterectomy for chronic, major-vessel thromboembolic pulmonary hypertension. After operation the patient developed reperfusion oedema and hypoxaemia which was treated successfully with inhalation of nitric oxide. Before operation, the response to inhaled nitric oxide was characterized by a slight reduction in pulmonary vascular resistance but without improvement in gas exchange. The postoperative improvement in oxygenation after inhalation of nitric oxide contrasted sharply with the preoperative reaction.
Endocarditis is a rare complication of brucellosis, often fatal, and the treatment is controversial. We present a case of Brucella melitensis endocarditis successfully treated by a combination of surgical resection and antibiotics.
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Confluent endothelialisation of vascular grafts in vitro before implantation has been suggested as a way to improve patency. With the aim of creating a confluent endothelium or expanded polytetrafluoroethylene (ePTFE) vascular grafts, using a minimum of allo- or xenogenic material, we have investigated the use of human serum for endothelial cell (EC) growth and adhesion to the grafts. Loss of fibronectin from the serum was measured before and after coating. After serum- or collagen I-precoating, the grafts were seeded with cultured adult human endothelial cells from the great saphenous vein and then kept under rotational culture conditions for 2 days. To evaluate the endothelial resistance to detachment the grafts were mounted in parallel to a heart-lung machine, delivering a pulsatile flow of human blood for 1 hour. Evaluation was performed using scanning electron microscopy (SEM). By simply pressing serum through the graft wall, fibronectin corresponding to 19 micrograms/cm2 graft surface was consumed. It was possible to achieve a confluent endothelium on both serum- and collagen I-precoated grafts (n = 8). After being subjected to blood flow, SEM revealed a complete endothelial lining of the grafts (n = 12) except for two serum-precoated grafts which showed < or = 10% and between 10 and 20% denuded areas, and one collagen-coated graft that showed < or = 10% of denuded area. This method provides a way to achieve a confluent and flow resistant endothelial lining on ePTFE vascular grafts.
Episodes of atrial fibrillation or flutter frequently complicate the postoperative course after coronary bypass surgery. A hundred and one patients undergoing coronary artery bypass surgery were randomized to oral pre- and postoperative treatment with sotalol, a non-selective beta-blocking agent with class-III antiarrhythmic properties (50 patients), or to half the preoperative beta-blocking dose according to the routine of the department (51 patients). Thus, there was no equipotency regarding beta blockade in the two groups. The incidence of atrial fibrillation was 10% in the sotalol group and 29% in the comparison group, p = 0.028. In 10% of the sotalol patients the dose had to be reduced or stopped compared to in none the group given routine treatment. The patients who developed atrial fibrillation were older, but otherwise there was no statistically significant difference between the two groups. Sotalol was effective in reducing the incidence of atrial fibrillation. However, careful titration of the optimal dose should be performed in order to avoid side effects of the beta blockade.
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A 68-year-old man with recurrent attacks of monomorphic ventricular tachycardia (VT) received a pacer cardioverter defibrillator featuring antitachycardia pacing and cardioversion/defibrillation. Over 300 episodes of VT were successfully terminated by antitachycardia pacing. During Holter monitoring the patient experienced supraventricular tachycardia with delivery of multiple antitachycardia pacing, cardioversion, and defibrillation therapies ending with the death of the patient. The following factors played a role in the unfortunate outcome of this patient: 1. triggering of VT therapy by an unexpected high sinus rate; 2. atrial fibrillation induced by cardioversion therapy; 3. a gradual and continuous increase in rate during atrial fibrillation possibly caused by repeated VT and ventricular fibrillation therapies and/or by a thrombus, found at autopsy, in a bypass graft; and 4. the limited ability of presently available defibrillators to distinguish between ventricular and supraventricular arrhythmias.
During a 6-year period (1983-1988), 1137 patients underwent surgery which included replacement of the aortic valve. There were 73 deaths within 30 days of surgery. A retrospective analysis showed that in four cases the cause of death probably was related to intraoperative damage to the right coronary artery, which in three cases was accidentally obstructed by a suture and in the fourth case was found at autopsy to be occluded by an organized thrombus. None of the four patients died intraoperatively. Death occurred 2 hours to 20 days postoperatively from arrhythmia and/or pump failure caused by myocardial infarction.
A series of 135 adults undergoing cardiac surgery was randomized to an autotransfusion group (n = 67) or a control group (n = 68). In the autotransfusion group mediastinal blood was collected and reinfused during the first 6 postoperative hours. Blood from the reservoir was taken for bacteriologic culture at the end of that time. The postoperative blood was comparable in the two groups. The average requirement of bank blood was 2.7 units in the autotransfusion group and 3.3 units in the controls (p less than 0.05). The average volume of autotransfusion blood was 336 ml. There were no clinical infections in the autotransfusion group, although 19% of the cultures were positive, and no apparent alteration of the coagulation mechanisms arose from infusion of autologous blood. No clinically significant intergroup differences were found in hematologic, renal or hepatic parameters, neurologic function or use of antibiotics.
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Twenty patients undergoing cardiac operations were randomly assigned to two protocols for heparin neutralization by protamine after cardiopulmonary bypass. In all patients protamine chloride was given at a ratio of 1 unit of protamine to 1 unit of injected heparin. In Group I (10 patients) all protamine was infused within 10 minutes after termination of cardiopulmonary bypass. Group II (10 patients) received 75% of the calculated protamine dose within 10 minutes after termination of bypass and the remainder after transfusion of all blood in the heart-lung machine. Plasma heparin levels were significantly lower in Group II 5 minutes after transfusion of all blood in the heart-lung machine and were 0.13 units/ml (standard deviation 0.04) in Group I and 0.06 units/ml (standard deviation 0.05) in Group II (p less than 0.001) 60 minutes after bypass. Activated partial thromboplastin time mirrored the changes in plasma heparin, whereas activated clotting time (Hemochron) was too insensitive to detect these low plasma heparin levels. We conclude that the two-dose protocol resulted in more complete heparin neutralization than the one-dose protocol.
Cerebral blood flow and metabolism of oxygen, glucose, and lactate were studied in 43 patients undergoing aortocoronary bypass. Twenty-five patients received prostacyclin infusion, 50 ng per kilogram of body weight per minute, during cardiopulmonary bypass (CPB), and 18 patients served as a control group. Regional cerebral blood flow (CBF) was studied by intraarterially injected xenon 133 and a single scintillation detector. Oxygen tension, carbon dioxide tension, oxygen saturation, glucose, and lactate were measured in arterial and cerebral venous blood. Mean arterial blood pressure decreased during hypothermia and prostacyclin infusion to less than 30 mm Hg. The regional CBF was, on average, 22 (standard deviation [SD] 4) ml/100 gm/min before CPB. It increased in the control group during hypothermia to 34 (SD 12) ml/100 gm/min, but decreased in the prostacyclin group to 15 (SD 5) ml/100 gm/min. It increased during rewarming in the prostacyclin group. After CPB, regional CBF was about 40 ml/100 gm/min in both groups. The cerebral arteriovenous oxygen pressure difference decreased more in the control group than in the prostacyclin group during hypothermia. The cerebral metabolic rate of oxygen decreased in both groups from approximately 2 ml/100 gm/min to about 1 ml/100 gm/min during hypothermia, increased again during rewarming, and after CPB was at the levels measured before bypass in both groups. There was no difference between the groups in regard to glucose and lactate metabolism.
Infusion of prostacyclin inhibits platelet activation during cardiopulmonary bypass (CPB) but also results in systemic arterial hypotension. Therefore, the effects of CPB and prostacyclin on renal function were studied in 36 male patients undergoing aortocoronary bypass. Nineteen patients (Group 1) received prostacyclin, 50 ng per kilogram of body weight per minute, during CPB, and 17 patients (Group 2) served as controls. There was pronounced hypotension in Group 1 only. Urine production during CPB averaged 88 +/- 140 ml and 2,306 +/- 1,112 ml in Groups 1 and 2, respectively. No patient had renal failure. Glomerular filtration rate (GFR), as measured by clearance of chromium 51-labeled ethylenediaminetetraacetic acid, was increased in Group 1 from 86 +/- 14 to 99 +/- 22 ml/1.73 m2/min (p less than 0.05) the day after operation, but remained unchanged in Group 2 (81 +/- 15 to 82 +/- 21 ml/1.73 m2/min). The increased GFR in Group 1 can be regarded as an expected adaptation to the change in body fluids after CPB. Therefore, the unchanged GFR in Group 2 must be regarded as caused by insufficient adaptation or impaired renal function. Proximal tubular function was evaluated by determination of beta 2-microglobulin in urine. In both groups, urinary beta 2-microglobulin and the ratio of urinary beta 2-microglobulin to urinary creatinine were increased the day after operation. The hypotension in Group 1 did not exacerbate the damage to tubular function.
Infusion of prostacyclin during cardiopulmonary bypass (CPB) reduces platelet activation, diminishes postoperative blood loss and decreases arterial blood pressure. In spite of continuous prostacyclin infusion, there is a delayed gradual rise in arterial pressure and resistance from low initial levels. We measured epinephrine (E), norepinephrine (NE), serotonin (5-HT), angiotensin II (ATII) and arginine-vasopressin (AVP) in plasma and carried out hemodynamic studies in 19 patients operated for coronary vascular disease. Eight patients served as a control group and were subjected to routine CPB. Eleven patients received prostacyclin 50 ng/kg/min during CPB. E and NE increased four- to sixfold during CPB from about 0.5 ng/ml (P less than 0.001). There was no difference between the groups. During CPB AVP increased sixfold from about 20 pg/ml in both groups (P less than 0.001), decreased early after CPB and increased again to high levels 3 h after CPB. The combined action of E, NE and AVP is of likely importance for the rise in systemic vascular resistance and/or need of vasodilation during CPB in the control group. ATII did not increase in the control group, but increased fourfold to about 20 pg/ml (P less than 0.01) during CPB in the prostacyclin group. The addition of AT II to E, NE and AVP seems responsible for the gradual return of arterial pressure and resistance during prostacyclin infusion. Postoperative hypertension and/or need of vasodilation 3 h after CPB was associated with high AVP levels in both groups. Hypotension caused by prostacyclin infusion did not increase E, NE or AVP above levels produced by CPB and moderate hypotension alone.
Somatosensory evoked potentials and cerebral metabolism were studied during cardiopulmonary bypass in 41 patients undergoing coronary bypass. Twenty-two patients received prostacyclin 50 ng/kg/min during cardiopulmonary bypass for platelet protection and 19 patients served as controls. Mean arterial blood pressure in the prostacyclin group was below 30 mm Hg during the first 30 minutes of bypass, but it remained above 50 mm Hg in the control group. Central conduction time, a measure of the electrical conduction time in the central nervous system, was prolonged in both groups during bypass up to 30 minutes of rewarming. The prolongation was greater in the control group early during bypass. At 20 minutes of cardiopulmonary bypass, central conduction time was increased by 81% (standard deviation 38) of the prebypass value in the control group and by 44% (standard deviation 17) in the prostacyclin group (p less than 0.001). Arteriovenous oxygen difference across the brain was greater in the prostacyclin group early during bypass. It was 36 ml/L (standard deviation 9) in the control group and 60 ml/L (standard deviation 18) in the prostacyclin group (p less than 0.001) at 10 minutes of bypass. There was no difference between the groups in regard to glucose and lactate. We conclude that cardiopulmonary bypass with hypothermia prolongs central conduction time. The hypotension induced by prostacyclin (50 ng/kg/min) did not further impair conduction in the central nervous system.
Twenty patients undergoing aorto-coronary bypass were randomly assigned to a prostacyclin treatment group or control group. Eight patients received 2 mg/kg heparin and 10 ng/kg/min prostacyclin before cardiopulmonary bypass (CPB) and 50 ng/kg/min during CPB. Twelve patients, serving as controls, received 3 mg/kg heparin. Heparinization resulted in a slight but significant increase of plasma beta-thromboglobulin in the control group but not in the prostacyclin group, and of plasma platelet factor 4 (PF-4) in both groups. After 90 minutes of CPB, beta-thromboglobulin was 408 (SD 128) ng/ml in the control group and 111 (SD 50) ng/ml (p less than 0.001) in the prostacyclin group. Platelet count, corrected for hemodilution, was 92% (SD 10) of the pre-CPB value after 10 minutes of CPB and 89% (SD 7) one hour after CPB in the control group, as compared to 113% (SD 10) and 145% (SD 18), respectively, in the prostacyclin group. Prostacyclin infusion before CPB reduced systemic vascular resistance to half of that of the control group, lowered mean arterial blood pressure, and increased cardiac index by 60% to 80%. An infusion of prostacyclin before CPB does not add to the already excellent platelet protective effect of 50 ng/kg/min prostacyclin during CPB, but may be used for vasodilation.