Family life: the long shadow of a sibling.
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Biomedical subjects
Publications and source records attributed to S Fox.
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Vertigo, lightheadedness, syncope, and hypotension occurring after implantation of a ventricular pacemaker has become known as pacemaker syndrome. In one patient with this syndrome we have demonstrated an associated decrease in the pulse amplitude of the ophthalmic arteries during ventricular pacing by utilizing ocular pneumoplethysmography (O.P.G.). This non-invasive technique was subsequently used intra-operatively to test the presence of ophthalmic artery pulse amplitude changes after implantation of the ventricular electrode. An A-V sequential pacemaker was then implanted and eliminated all symptoms of pacemaker syndrome.
The use of physiologic pacing utilizing transvenous atrial and ventricular electrodes has recently taken on increased importance. A simple, safe, technique for electrode implantation has been used in 14 patients and enabled the implanting physicians to establish permanent atrioventricular (A-V) sequential pacing with low risk in a short span of time.
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A recent review of 25 patients who had repair of coarctation of the aorta at the Milton S. Hershey Medical Center revealed a 56% incidence of paradoxical hypertension in the immediate postoperative period. Analysis of results from recent animal experiments helped us to formulate a logical explanation of the pathogenesis of this hypertension. Stimulation of sympathetic nerve fibers located between the media and adventitia of the aortic isthmus has two effects, both of which result in hypertension. The first effect is release of norepinephrine and consequential rise in systemic blood pressure. Second, this spinal reflex directly stimulates the juxtaglomerular cells to release renin and cause additional hypertension. An additional effect of this increased renin production might be the shunting of blood from mesenteric arteries, thus causing the abdominal symptoms of so-called post-coarctectomy syndrome. The inability of some patients to adapt to this spinal reflex may be related to the age of the patient when the coarctation was repaired. This probably explains the high incidence of persistent hypertension in patients who undergo coarctation repair after adolescence.
The motor function of the antrum was studied in 7 normal subjects, 4 patients with diabetes without GI symptoms, and 7 patients with diabetic gastroparesis. Both the number of antral contractions and the cumulative antral activity (percent of time during which the antrum contracted) in patients with diabetic gastroparesis were significantly lower than in normal subjects and diabetic patients without gastroparesis (P less than 0.01). Interdigestive motor complexes were observed in all normal subjects, but they were not present in any patients with diabetic gastroparesis. Intravenous metoclopramide did not affect the rate of antral contractions (P less than 0.1), but it increased the cumulative antral activity (P less than 0.001) in normal subjects and diabetics without gastroparesis. Metoclopramide, however, did not alter the rate of antral contractions (P less than 0.09) or the total cumulative antral activity (P less than 0.09) in diabetic patients with gastroparesis. Furthermore, in normal subjects, the action of metoclopramide was blocked by atropine sulfate (P less than 0.003). Bethanechol caused a slight increase in the number of antral contractions (P less than 0.05) and cumulative antral activity (P less than 0.01) in normal subjects. This cholinergic drug caused a marked increase in the rate of antral contractions and the cumulative antral activity in diabetic patients with gastroparesis. Antral contractions and cumulative antral activity were restored by bethanechol to normal values. These findings suggest a variable degree of gastric neuropathy in individual patients with diabetic gastroparesis with functionally intact antral muscles as assessed by their pharmacologic response to cholinergic stimulation.
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Traumatic aortic rupture is a common occurrence associated with 16 percent of deaths from automobile accidents. Through a review of current literature and two recent cases from The Milton S. Hershey Medical Center, we have attempted to elucidate a common physical finding, acute hypertension associated with blunt chest trauma, and prove its significance as a diagnostic clue to traumatic rupture of the aorta. New laboratory findings of an aortic sympathetic reflex stimulated by stretching the aortic wall in the area of the isthmus provides a physiological explanation for the cause of hypertension after aortic trauma.
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Staphylococcus aureus aortic valve endocarditis and its complications in a patient were readily recognized by echocardiography. "Shaggy" echoes recorded from the aortic leaflets in diastole as well as irregular diastolic densities in the left ventricular outflow tract suggested flail aortic leaflets secondary to bacterial endocarditis. The presence of a double echo of the anterior aortic wall was an unusual finding. Initially thought to represent a localized dissection, abscess formation and pocket of edematous fluid accumulation was found between the anterior aortic wall and pulmonary artery. Premature closure of the mitral valve was evident shortly before the patient died. The specific echocardiographic features of flail aortic leaflets and premature mitral valve closure should alert the physician to consider immediate aortic valve replacement.
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