Faculty Bibliography

Injury to the anterior cruciate ligament removes the major stabilizing structure to anterior tibial translation. The initial trauma may lead to meniscal and cartilage damage, predisposing the knee to early degenerative changes. Moreover, a knee with an isolated ACL rupture may have recurrent episodes of instability that can lead to a similar degenerative course. At this time, one cannot accurately predict which patients will tolerate ACL deficiency, and which patients will not. Current long-term studies support a progressive worsening condition in the ACL and meniscal deficient knees. Physical therapy together with lifestyle modifications may be necessary. Those unwilling to make these types of changes or those with associated injuries may benefit from ACL reconstruction

HYPOTHESIS: Similar to familial tumors, sporadic head and neck paragangliomas are associated with chromosomal deletions at either 11q13 or 11q22-23. BACKGROUND: Familial paragangliomas are inherited in an autosomal dominant pattern with genomic imprinting of the maternal allele. Genetic studies of familial paragangliomas have localized the causative genetic defect to two separate loci: 11q13.1 and 11q22-23. The molecular pathogenesis of sporadic head and neck paragangliomas has not been studied. METHODS: Blood and tumor samples from patients with sporadic head and neck paragangliomas were screened for deletions on chromosome 11 using DNA microsatellite markers and polymerase chain reaction. Polymerase chain reaction-amplified alleles from tumor specimens were compared with those from the blood of eight patients. A greater than 50% reduction in band intensity (as determined by densitometric analysis) between blood and tumor sample was indicative of a chromosomal deletion. RESULTS: Three of the eight patients were found to have deletions at chromosome 11q: two at chromosome 11q22-23 and one at 11q13. CONCLUSIONS: Sporadic head and neck paragangliomas are associated with deletions at chromosome 11q13 and 11q22-23. It is thus likely that sporadic and familial paragangliomas share a similar molecular pathogenesis.

The changes that occur in the body as part of the normal aging process and the degenerative changes that often accompany them predispose the elderly to various orthopedic problems. Age, general health, and functional level are all important factors in determining the optimum management of these patients. Treatments are aimed at restoring patient independence and activity to preinjury levels, while at the same time minimizing the risks of treatment complications

BACKGROUND: Ventricular pressure and volume overload may induce hemodynamically important ventricular interactions mediated by the thick interventricular septum. The purpose of this study was to determine whether analogous hemodynamically manifest atrial interactions occur across the thinner interatrial septum. METHODS: Right atrial (RA) and left atrial (LA) pressures were measured with micromanometer-tipped catheters before and after atrial pressure and volume overload elicited by sequential right ventricular (RV), RA, and septal ischemia induced in nine open-chest dogs. RESULTS: Following RV ischemia, RA pressure increased and RA contraction and relaxation were enhanced, as indicated by an augmented A wave and X descent. Despite decreased LV diastolic size, LA pressure increased, with similar increases in its A wave and X descent. RA ischemia depressed RA contraction and relaxation, resulting in diminished A wave and X descent. Parallel changes occurred in the LA waveform. Following septal ischemia, LA contraction and relaxation were enhanced, as reflected in an augmented A wave and X descent. Despite persistent RA ischemia, the RA A wave and X descent increased. CONCLUSIONS: These findings demonstrate interatrial transmission of pressure and waveform changes that may influence hemodynamic evaluation and cardiac function.

To determine whether modulation of systolic ventricular interaction influences right ventricular performance during right heart ischemia, the effects of septal ischemia and inotropic stimulation were studied in 15 dogs in an open chest preparation. Right coronary branch occlusions led to right ventricular dilation and free wall dyskinesia, reversed septal curvature and reduced left ventricular diastolic volume. In systole, the septum thickened but bulged paradoxically into the right ventricle generating an active but depressed right ventricular systolic pressure (28.9 +/- 5.5 to 22.1 +/- 4.5 mm Hg), with associated decreases in right ventricular stroke work (5.66 +/- 0.94 to 1.92 +/- 0.53 g.m/m2) and left ventricular systolic pressure (123 +/- 11 to 80 +/- 10 mm Hg). Septal ischemia induced systolic septal thinning, left ventricular dilation and decreased left ventricular systolic pressure (80 +/- 10 to 55 +/- 10 mm Hg) and stroke work. Although the extent of paradoxic septal displacement increased, there were further decrements in right ventricular systolic pressure (22.1 +/- 4.5 to 18.7 +/- 4.3 mm Hg) and stroke work (1.92 +/- 0.53 to 0.7 +/- 0.2 g.m/m2). Dopamine infusion augmented left ventricular free wall contraction and increased left ventricular systolic pressure (55 +/- 10 to 172 +/- 17 mm Hg) and stroke work. Although systolic septal thinning persisted, the extent of paradoxic septal displacement increased strikingly and, despite continued right ventricular free wall dyskinesia, right ventricular systolic pressure increased (18.7 +/- 4.3 to 39.6 +/- 6.2 mm Hg) as did right ventricular stroke work (0.7 +/- 0.2 to 7 +/- 1.6 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the importance of right atrial function with acute right ventricular dysfunction, sequential right ventricular and right atrial ischemia were induced in 15 dogs. Right ventricular ischemia resulted in right ventricular free wall dyskinesia, right ventricular dilation by ultrasound, elevated right ventricular filling pressure and paradoxic septal motion. There were decrements in right ventricular systolic pressure (28.9 +/- 5.5 to 25.5 +/- 4.6 mm Hg) (p less than 0.05 for these and all subsequent values) and stroke work (5.66 +/- 0.94 to 2.66 +/- 0.62 g.m/m2), resulting in reductions in left ventricular preload, systolic pressure (123 +/- 11 to 97 +/- 12 mm Hg) and stroke volume (24.2 +/- 4.3 to 19.1 +/- 5.2 ml). Right atrial contractility was augmented, as indicated by increases in peak A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.22 +/- 0.02 to 1.46 +/- 0.3) and right atrial stroke work (0.11 +/- 0.02 to 0.25 +/- 0.05 g.m/m2). Right atrial ischemia depressed right atrial contraction, as indicated by decreased A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.46 +/- 0.3 to 1.04 +/- 0.2) and stroke work (0.25 +/- 0.05 to 0.04 +/- 0.01 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)