Late presentation and successful treatment of classical scimitar syndrome.

Scimitar syndrome is a form of partial anomalous pulmonary venous drainage that is dramatically visible on plain chest radiography (CXR). In these individuals the entire venous drainage from the right lung enters a single anomalous large vein that descends to the inferior vena cava. This descending vein is visible on CXR as a curvilinear density along the right heart border and resembles the curved Turkish sword that gives the condition its name. Scimitar syndrome forms part of the large spectrum of associated conditions known as venolobar syndrome. These include right lung hypoplasia or sequestered segments of right lung, congenital heart disease and various others. We report the case of a young woman who presented incidentally, with a murmur, at 16 years of age. Full investigation including angiography showed a large atrial septal defect with right heart dilation and scimitar syndrome. She underwent surgical correction with uneventful and complete correction by baffling of the scimitar vein from its entry into the inferior vena to the left atrium through the enlarged atrial septal defect.

Tolerance to ACE inhibitors after cardiac surgery.

OBJECTIVES: Several studies have shown angiotensin-converting enzyme (ACE) inhibitors to confer significant mortality and morbidity benefits in heart failure. First-dose hypotension may necessitate interruption of such therapy. This is more likely to occur if the ACE inhibitor is administered early after coronary artery bypass grafting (CABG). The purpose of this study was to analyse the haemodynamic tolerance to early post-operative treatment with perindopril and enalapril in patients with impaired renal and ventricular function. METHODS: Eighty one consecutive CABG patients with a previous myocardial infarction, impaired pre-operative left ventricular ejection fraction (LVEF) on ventriculography and moderately impaired renal function (serum creatinine of 115-150 micromol/l) were randomised into three groups to receive oral placebo, perindopril (4 mg) or enalapril (5 mg) once daily. Groups were subdivided into those with mild ventricular dysfunction (LVEF = 35-65%, n = 20) and significant ventricular dysfunction (LVEF < 35%, n = 7). Exclusion criteria included oliguria (<0.5 ml/kg per h) or inotrope dependance at the point of entry on the first post-operative day. Intolerance to ACE inhibitor was defined as hypotension (<95 mmHg systolic blood pressure or a decrease exceeding 25 mmHg in systolic blood pressure) leading to oliguria (<0.5 ml/kg per h) which was unresponsive to intravenous furosemide (20 mg). In such cases ACE inhibitor treatment was discontinued and patients commenced on dopamine. RESULTS: In the groups with mild ventricular dysfunction (LVEF = 35-65%) perindopril was discontinued in 1/20 and enalapril in 4/20 patients (P = n.s). However, in the groups with significant ventricular dysfunction (LVEF < 35%) perindopril was discontinued in 2/7 and enalapril in 7/7 patients (P = 0.02). CONCLUSION: Our results suggest that after CABG, patients with moderately impaired renal function and significant ventricular dysfunction do not tolerate ACE inhibitors well when these were commenced on the first post-operative day. However, perindopril was associated with less haemodynamic deterioration than enalapril and consequently may be advantageous in this setting. rights reserved.

Repair of torn pulmonary artery in redo operation.

Intraoperative pulmonary artery tears may complicate redo cardiac operations. We report a method of repair for these tears occurring in 2 patients undergoing second redo mitral valve operation by performing transection of the aorta and primary repair of the tear. This is a safe rapid procedure which gives excellent results.

Expression of soluble endothelial adhesion molecules in clinical cardiopulmonary bypass.

Soluble endothelial adhesion molecule expression in clinical cardiopulmonary bypass (CPB) was investigated. Neutrophil-mediated endothelial injury plays an important role in CPB-induced organ dysfunction. The adhesion of neutrophil to the endothelium is central to this process. It has been well documented that CPB induces neutrophil activation and changes in neutrophil adhesion molecule expression, but the effect of CPB on endothelial cell activation is not known. This study was designed to measure soluble endothelial adhesion molecules during CPB. We made serial measurements (by specific enzyme-linked immunoabsorbent assay) of plasma levels of the soluble endothelial adhesion molecules, ICAM-1 and E-selectin in patients undergoing routine CPB (n = 7) and in a control group (thoracotomy, n = 3). The results show an initial significant decrease during CPB followed by an increase in plasma E-selectin from 29.3 +/- 5.1 ng/ml (mean +/- SEM) prebypass to 34.0 +/- 5.4 ng/ml at 48 h postbypass. Likewise, plasma ICAM-1 significantly decreased during CPB and then increased from 246.3 +/- 38.0 ng/ml before bypass to 324.8 +/- 25.0 ng/ml and 355.0 +/- 23.0 ng/ml at 24 and 48 h after bypass, respectively. The rise in levels is statistically significant (p < 0.05). This study shows a decrease in circulating ICAM-1 and soluble E-selectin during CPB and an increase in their levels at 48 h after CPB.

Pleural effusion associated with D-penicillamine therapy: a case report.

This case report illustrates the occurrence of a large pleural effusion associated with long-term D-penicillamine therapy. This complication has not previously been reported.

Dynamics of early postischemic myocardial functional recovery. Evidence of reperfusion-induced injury?

BACKGROUND: The present study was designed to explore the relation between the duration of ischemia and the rate and extent of myocardial functional recovery after reperfusion. METHODS AND RESULTS: Isolated rat hearts were perfused with blood from a support animal for 15 minutes (flow rate, 2.5 mL/min; perfusion pressure, 60.1 +/- 1.3 mm Hg). Control left ventricular developed pressure (LVDP) was measured, and the hearts (six per group) were subjected to 10, 20, 30, 40, 50, 60, 70, or 80 minutes of global ischemia (37 degrees C) and 60 minutes of reperfusion. Pacing (320 beats per minute) was instituted before and after ischemia. In all groups, transient arrhythmias occurred at the onset of reperfusion, to be followed by an early phase of recovery that peaked after 2 to 3 minutes of reperfusion. The relation between the extent of this initial recovery and the duration of preceding ischemia was described by a bell-shaped curve. Thus, the maximum initial mean recovery after 10, 20, 30, 40, 50, 60, 70, or 80 minutes of ischemia was 97%, 108%, 145%, 154%, 118%, 34%, 41%, and 24%, respectively, of preischemic LVDP. Possibly indicative of reperfusion-induced injury, LVDP then declined in all groups so that after 20 minutes of reperfusion, the mean recovery was 63%, 53%, 48%, 50%, 56%, 12%, 9%, and 5%, respectively. In the 10-, 20-, 30-, and 40-minute ischemia groups, there then was a secondary increase in LVDP, possibly indicating the start of recovery from stunning. After 60 minutes of reperfusion, the mean recovery of LVDP was 82%, 65%, 59%, 54%, 47%, 9%, 7%, and 4%, respectively; this second phase of recovery was inversely proportional to the duration of ischemia. To define the early phase of recovery that had been obscured by reperfusion-induced arrhythmias, we repeated the experiments with the inclusion of a cardioplegic infusion (St Thomas' solution for 2 minutes before ischemia). This significantly reduced the incidence of ventricular fibrillation during early reperfusion. The extent of the initial postischemic recovery of LVDP was similar to that observed without cardioplegia; however, the mean secondary recovery was greater in all groups. Again, the relation of early transient (2 to 5 minutes) recovery to the duration of ischemia was represented by a bell-shaped curve, whereas the secondary recovery was inversely related. CONCLUSIONS: Although the results of the present study confirm the protective properties of cardioplegia, they also shed some light on the nature of reperfusion-induced injury and myocardial stunning and their complex relation to the severity of the preceding ischemia.

An unusual case of supraventricular arrhythmia.

This case report describes the occurrence of a supraventricular arrhythmia in a patient with a large epiphrenic oesophageal diverticulum. The arrhythmia was precipitated by meals and was thought to result from pressure effects on the left atrium. Medical therapy did not control the arrhythmia. Excision of the diverticulum combined with oesophageal myotomy resulted in a dramatic relief of symptoms.

Omission of aspirin in patients following coronary artery bypass graft surgery.

Graft patency is a major factor contributing to the long-term results of coronary artery bypass graft (CABG) surgery. The systematic overview of the Antiplatelet Trialists' Collaboration provides unequivocal evidence that antiplatelet therapy reduces by nearly one-half the odds of coronary graft occlusion following CABG. We retrospectively reviewed patients undergoing CABG during 1993 at the Cardiothoracic Unit, Northern General Hospital, to determine the incidence of, and indications for, aspirin omission following CABG: 462 patients with isolated CABG, 75 patients with a combined CABG and a heart valve procedure and 21 patients with a combined CABG and other non-valve procedure. Thirty-six patients (7.5%) with isolated CABG and CABG combined with a non-valve procedure were not prescribed aspirin. The reasons for aspirin omission were categorized into three groups depending on whether omission was fully justified (group 1), possibly justified (group 2) or unjustified (group 3). Twenty-one patients were in groups 2 and 3, nine of whom were started on aspirin 2-6 weeks after discharge without any ill effect. Forty-two patients were discharged from hospital on a three month course of warfarin. Four months later four patients had died, 24 had changed to aspirin, 10 were still on warfarin and four were on neither drug. Aspirin was sometimes omitted without clear indications. Better provisions for supervision should be made by either the General Practitioner or Hospital Practitioner during the change-over period from oral anticoagulation to antiplatelet therapy in patients on a short course of warfarin.

Thromboxane A2 mediates pulmonary hypertension after cardiopulmonary bypass in the rabbit.

Clinically, it is well established that cardiopulmonary bypass results in pulmonary dysfunction. Using a recently developed preparation for cardiopulmonary bypass in the rabbit, we have been able to mimic a similar, but more severe, condition. We found that, despite normal histologic structure of the myocardium, hearts could not be weaned from bypass because of a serious increase in pulmonary vascular resistance. Histologic studies of the lungs showed severe intravascular neutrophil aggregation and marked vasoconstriction. To identify the nature and origin of the mediator responsible for the changes in the pulmonary vasculature, we subjected groups of rabbits (n = 4 per group) to bypass with cooling to 18 degrees C, circulatory arrest for 1 hour, and rewarming on bypass to 33 degrees C. Pulmonary vascular resistance was measured at the same temperature before and after bypass. Four groups were studied: group I were untreated controls; group II received the cyclooxygenase inhibitor, indomethacin (0.2 mg/kg intravenously), before operation; group III received the thromboxane A2 synthetase inhibitor, Dazmegral (5 mg/kg intravenously), before operation together with the thromboxane A2 receptor blocker GR 32191B (2 mg/kg per 30 minutes intravenously); and group IV were treated with mustine hydrochloride (1.75 mg/kg intravenously) 3 days before the experiment to deplete the neutrophils by 90%. During circulatory arrest, the heart was protected with an initial infusion (10 ml at 4 degrees C over 1 minute) of St. Thomas' Hospital cardioplegic solution. At the end of the experiment, the heart and lungs were histologically examined. In the control group, a significant increase (+395% when compared with the value recorded before bypass) in pulmonary vascular resistance was observed after bypass. However, in none of the treated groups did pulmonary vascular resistance increase significantly (percentage changes in groups II, III, and IV were -24%, 0%, and +33%, respectively). Pulmonary histologic characteristics were normal in all treated groups, and all animals were successfully weaned from bypass. These results indicate that the increase in pulmonary vascular resistance that arises as a consequence of bypass in rabbits is primarily a result of the production of thromboxane A2, a process in which the neutrophil plays a pivotal role.

Double aortic arch causing tracheoesophageal compression.

Since 1972, 17 patients have been surgically treated for double aortic arch at our institution. The procedure became necessary before 12 months of age in 11 patients and before 24 months in 16 patients. The major symptoms were respiratory distress, noisy breathing, and respiratory infections; four patients also had dysphagia. A high degree of clinical suspicion should warrant further investigation. Barium swallow and bronchoscopy were diagnostic and revealed extrinsic compression of the esophagus and trachea, respectively. Division of the anterior arch was performed in 16 patients; the right (posterior) arch was divided in the remaining patient. Kommerell's diverticulum was found in four patients and was resected in order to avoid recurrence of dysphagia by compression. A vascular suspension procedure was necessary in 13 patients to further release the trachea and esophagus. There was no mortality in this series, and symptomatic improvement was achieved in all patients. A degree of tracheomalacia may be responsible for some residual symptoms in four patients.

Contractile and vascular consequences of blood versus crystalloid cardioplegia in the isolated blood-perfused rat heart.

The protective effects of sanguineous and asanguineous St. Thomas' cardioplegia (SCP and ACP) on post-ischemic vasodilator responsiveness, left ventricular developed pressure and end-diastolic pressure (LVDP and LVEDP), tissue adenosine triphosphate (ATP) and creatine phosphate (CP) contents were compared in the isolated blood-perfused rat heart. Five groups of hearts were studied: the controls (n = 8) perfused with blood (from a support rat) for 50 min (37 degrees C), versus hearts (n = 14/group) arrested by a single infusion of either cardioplegic solution (15 degrees C) prior to global ischemia (15 degrees C) and blood reperfusion (37 degrees C). After 2 or 4 h of ischemia and 50 min of reperfusion, endothelium-dependent vasodilator acetylcholine (1 microgram) induced a 10 +/- 0.5 and 8.5 +/- 0.5% reduction, respectively, in coronary resistance, in the SCP groups, but only a 6.5 +/- 0.6 and 4.5 +/- 0.5% reduction (P < 0.05), respectively, in the ACP groups. However, there were no significant differences in LVDP, LVEDP, tissue ATP and CP contents, and endothelium-independent vasodilator response to nitroglycerin between the two cardioplegic groups. In a further study, rat hearts (n = 8/group) were arrested with SCP (magnesium concentration < 0.5, 5.0 or 16.0 mmol/l, in groups 1, 2 and 3) and subjected to 4 h of global ischemia (15 degrees C) followed by 50 min of blood reperfusion (37 degrees C). At the end of reperfusion, LVDP (at a ventricular volume of 180 microliters) was 60 +/- 3.4, 72 +/- 3.5 and 70 +/- 3.2 in groups 1, 2 and 3, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Extensive endocardial resection for recurrent ventricular tachyarrhythmias.

Twenty-two consecutive patients underwent elective map-guided extensive endocardial resection (EER) for recurrent ventricular tachyarrhythmias (VT) of whom 20 were male. The ages ranged from 43 to 74 years (mean 57). All arrhythmias were ischaemic in origin. The mean ejection fraction was 29%. The presenting arrhythmias were ventricular tachycardia in 14, ventricular fibrillation (VF) alone in 1 and ventricular tachycardia and VF in 7. Useful additional intraoperative mapping was obtained in 19 patients. Under cardioplegic arrest, the scarred left (22) and where indicated right (4) ventricular endocardium was extensively resected. Resection of scarred papillary muscles was avoided and where indicated, localised cryoablation was performed: 21/22 had concomitant aneurysmectomy and/or coronary artery bypass grafting. There was 1 (4.5%) operative death. All survivors (95.5%) underwent postoperative electrophysiological studies at around 1 week. None had inducible arrhythmias. There were 3 (13.5%) late cardiac deaths, all due to primary cardiac failure without recurrence of arrhythmia. Of 17 (77%) long-term survivors, 16 (94%) are VT-free on no anti-arrhythmic medication at a mean follow-up of 37.2 months. One developed a new arrhythmia at 1 year which is controlled on medication. EER offers a high rate of success in ablating VT in association with a low operative mortality and good prospect of VT-free long-term survival.

Erythrocyte fatty acid profiles in patients with bronchogenic carcinoma.

The use of the erythrocyte stearic:oleic acid ratio in the diagnosis and prognosis of bronchogenic carcinoma has been assessed. Although there was a significant difference (P less than 0.02) in the erythrocyte stearic:oleic acid ratio between bronchogenic carcinoma patients and healthy adults, the large overlap observed in the two groups rendered the test unsuitable for the diagnosis of malignancy. Furthermore, there was no consistent rise in this ratio after surgical resection, indicating the test to be of little prognostic use. A new explanation for the lower stearic:oleic acid ratios in certain patients has been postulated.