Two-vessel PTCA of single anomalous coronary artery.
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Biomedical subjects
Publications and source records attributed to S Amikam.
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This paper describes an approach to the treatment of exposed pacemaker generator and electrode. Local infection is controlled by the administration of systemic antibiotics and topical antibacterial solutions. Because the generator and lead are enveloped by an inert synthetic coating, it is possible to eradicate an infection without their removal if it is due to a weak opportunist pathogen fully sensitive to antibiotics. Thereafter, subcapsular relocation of the exposed generator or vertical-to-horizontal transposition of the exteriorised lead is carried out. These surgical interventions are designed to overcome the vertical force which tends to cause the extrusion of the pacing hardware.
A 65-year-old man with Behçet's disease developed transient complete A-V block with syncope. An attempt to implant a permanent transvenous endocardial electrode failed owing to obstructions in the subclavian, innominate, and superior vena cava veins demonstrated by angiography. Sutureless epicardial electrodes were successfully implanted through a subxyphoid approach. Obstruction in the great veins is a common feature in patients with Behçet's disease. We suggest that patients with this disorder, who require a permanent pacemaker, should be investigated by angiography prior to implant to rule out obstruction in the upper great veins.
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A 53-year-old patient with corrected transposition of the great arteries developed complete heart block with fainting episodes. After temporary pacing through the endocardium of the venous (anatomically left) ventricle, a permanent epicardial pacemaker was implanted. This case shows the progressive nature of the atrioventricular conduction disturbances, which are very common in association with this congenital cardiac anomaly.
Forty-four patients with sick sinue syndrome (SSS) who had been treated with a permanent pacemaker were followed for an average period of 39 months. Fifteen patients had bradyarrhythmia alone (group 1) and 29 had bradycardia-tachycardia syndrome (group 2). Eight patients, all from group 2, died within a short period following pacemaker implantation. They all had ischemic heart disease, congestive heart failure and a short history of the symptomatic dysrhythmia. Eleven patients developed stable chronic atrial fibrillation, which terminated the clinical syndrome. In the remaining 25 patients, all without evidence of ischemic heart disease, the dysrhythmia persisted although symptoms were successfully controlled following pacemaker therapy. Based on these observations and data obtained from other surveys, we delineated three courses of SSS: 1) a subacute course, characterized by a short-term survival; 2) a transient, self-limited course in which conversion to stable atrial fibrillation occurs; and 3) a chronic course, in which the dysrhythmia persists and permanent pacemaker therapy is indicated.
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The electron microscopic features of the striated skeletal muscle, the striated cardiac muscle, and the smooth muscle from a woman who had been suffering for many years from myotonia dystrophica with cardiac involvement are described. The skeletal muscle was studied at two different stages of the disease. In the first material the main changes consisted of centrally situated nuclei, disorganisation of the sarcomeres, and focal disruption of the Z-line. The satellite cells were well represented. Three years later atrophy and degenerative, necrotic changes of the skeletal muscle were evident. The satellite cells were absent. Few changes were seen in the striated cardiac muscle. These consisted of slight interstitial fibrosis and large accumulations of mitochondria with intramitochondrial dense granules. The smooth muscle cells of the oesophagus showed disorientated filaments and mild degenerative changes. It is concluded that the skeletal muscle was more severely affected than the other types of muscle.
Five children with polysplenia syndrome are described. Cardiac catheterization or postmortem examination revealed the following cardiac anomalies: interruption of the inferior vena cava with azygos (or hemiazygos) continuation to the left superior vena cava and a single atrium or a large atrial septal defect in all five children; a ventricular septal defect in three; and a primitive ventricle in one case. Other anomalies found were: central liver in all five; a right-sided stomach in three; and multiple small spleens and bilateral left, bilobed lungs--found on autopsy--in two of the children. In four of the five patients, whose ECG was available, a negative P wave was present in leads II, III and AVF. This leftward and superiorly directed P wave axis should suggest a diagnosis of polysplenia syndrome in an infant with congenital heart disease. The cardiac anomalies are surgically correctable; therefore, early recognition of this syndrome is of practical importance.
A patient is described in whom myopotentials orginating from the anterior abdominal wall muscle suppressed the implanted demand pacemaker despite its bipolar mode of action. This phenomenon was shown by simultaneous recording of the electrocardiogram the electromyogram. At operation, a defect in the insulation of a previously repaired epicardial electrode was found lying in close proximity to these muscles. After repair of the insulation defect, normal pacemaker function was restored. It is suggested that the myopotentials leaked into the pacing system through the insulation defect, thereby suppressing the demand unit, which maintained its bipolar mode of pacing throughout.
In 34 out of 36 patients with apical right ventricular endocardial pacing, primary ischaemic ST alterations were observed during the early stage of acute myocardial infarction. These ST changes, indicating acute injury, were detected in the paced beats in inferior and in anterior infarct. The primary ST changes were consistent only during the early stages of acute myocardial infarction and were not detected when the electrode tip was not in the apex of the right ventricle. It is suggested that the primary ST changes should be used to diagnose acute myocardial infarction in paced patients.
A 22-year-old woman with a right atrial myxoma prolapsing to the right ventricle is described. The haemodynamic findings were similar to those of cases of prolapsing myxoma of the left atrium; a notching on the ascending limb of the right ventricular pressure curve, and an initial negative, irregular deflection on the pulmonary artery pressure curve with a pronounced rise in the mean right atrial pressure (18 mmHg) were found. On deep inspiration there was a significant deepening of the y descent from 12 mmHg to 2 mmHg, indicating a changing, dynamic obstruction of the right ventricle inflow tract. These haemodynamic features can be helpful in the diagnosis of prolapsing right atrial myxoma.
A persistent left superior vena cava can complicate the implantation of a transvenous pacemaker. In a patient who required a permanent pacemaker, this venous anomaly was discovered during the insertion of the electrode but it did not prevent long-term right ventricular pacing. This was achieved after the electrode had been manipulated through the coronary sinus and right atrium. A plan of management is proposed for dealing with this unexpected problem.
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