Biomedical subjects

Brianne F Blumenthal

Publications and source records attributed to Brianne F Blumenthal.

4 recordsLinked to original sources

PubMed2004

Regional functional depression immediately after ventricular septal defect closure.

Left ventricular ejection is depressed immediately after repair of ventricular septal defect (VSD). Postrepair functional depression seen after VSD closure could result from a reduction in preload. However, other mechanisms could be at work. Functional depression could also be caused by closure of a low-impedance path for left ventricular ejection, the introduction of a stiff akinetic patch, or the operation itself. We reasoned that functional depression mediated by changes in preload or afterload should symmetrically affect end-diastole and end-systole, whereas depression resulting from changes in septal mechanics should be localized. We, therefore, performed segmental wall-motion analysis on intraoperative echocardiograms from patients undergoing VSD and atrial septal defect repair. After VSD closure, there was an asymmetric change in left ventricular end-systolic segment length and a decrease in fractional segment shortening localized to the septal and lateral walls, whereas patients with atrial septal defect had a symmetric increase in fractional shortening. These results suggest that acute functional depression after VSD repair is a result of localized impairment of septal function.

Cardiac Surgical Procedures↗

PubMed2004

Echocardiographic analysis of ventricular geometry and function during repair of congenital septal defects.

BACKGROUND: This study investigated changes in left ventricular (LV) geometry and systolic function after corrective surgery for atrial (ASD) and ventricular septal defects (VSD). METHODS: Transesophageal LV short-axis echocardiograms were recorded before and after operative repair of ASD (n = 11) and VSD (n = 7). Preload was measured using LV end-diastolic area indexed for body surface area. Measurements of septal-freewall (D1) and anterior-posterior (D2) endocardial diameters were used to assess LV symmetry from D1/D2. Systolic indices included stroke area, area ejection fraction, and fractional shortening. RESULTS: Preload, stroke area, area ejection fraction, and fractional shortening of D1 increased after ASD repair but decreased after VSD repair (p < 0.05). End-diastolic symmetry increased after ASD closure and decreased after VSD closure (p < 0.05). Increases in stroke area and ejection fraction after ASD correction primarily reflected increased shortening of D1. A positive correlation was found overall between percent change in end-diastolic area (EDA) and percent change in area ejection fraction (r(2) = 0.80, p < 0.0001, n = 18). CONCLUSIONS: Preload was the primary determinant of changes in LV function in this series of ASD and VSD repairs. Intraoperative changes in position of the interventricular septum affected systolic and diastolic LV symmetry and septal free wall shortening. Additional studies are needed to define changes in afterload and contractility as well as diastolic compliance and systolic mechanics.

Child↗

PubMed2002

Correlation of thrombophilia and hypofibrinolysis with pulmonary embolism following total hip arthroplasty: an analysis of genetic factors.

BACKGROUND: The increased thromboembolic risk associated with total hip arthroplasty is multifactorial. We assessed whether the prevalence of abnormalities shown by newer genetic screening tests for thrombophilia and hypofibrinolysis was higher in patients in whom pulmonary embolism had developed after total hip arthroplasty than it was in matched control patients. METHODS: Fourteen patients with documented pulmonary embolism after total hip arthroplasty and fourteen matched control patients who had undergone total hip arthroplasty without any clinical indication of thromboembolism were evaluated for risks of thrombophilia and hypofibrinolysis. Functional tests of hemostasis included evaluations of prothrombin time; activated partial thromboplastin time; levels of fibrinogen, serum homocysteine, protein C and S, and antithrombin III; activated protein-C resistance; and dilute Russell viper venom time. Molecular genetic testing was performed for factor-V Leiden, prothrombin promoter G20210A, methylenetetrahydrofolate reductase C677T, plasminogen activator inhibitor-1 4G/4G, and platelet glycoprotein IIb/IIIa A1/A2 or A2/A2 mutations. RESULTS: The total number of genetic thrombophilic abnormalities identified was higher in the pulmonary embolism group (twenty-four abnormalities) than in the control group (fifteen abnormalities). Only patients with pulmonary embolism were found to have heterozygosity or homozygosity for the prothrombin G20210A mutation (four of fourteen patients; p = 0.05 compared with the control group) and a decreased antithrombin-III level (three of thirteen patients; p = 0.10 compared with the control group). Patients with pulmonary embolism were much more likely than control patients to have at least one thrombophilic abnormality: seven of fourteen patients with pulmonary embolism had a low antithrombin-III level or the prothrombin G20210A gene mutation compared with none of the fourteen in the control group (Fisher exact test, p < 0.01). The presence of the prothrombin G20210A gene mutation was significantly correlated with pulmonary embolism (r = 0.41, p = 0.03), as was the presence of least one abnormality (a low antithrombin-III level or the presence of the prothrombin G20210A gene mutation) (r = 0.58, p = 0.001). CONCLUSIONS: Genetic thrombophilia and hypofibrinolysis were more frequent in patients who had had pulmonary embolism after total hip arthroplasty than in those who had not. The presence of multiple genetic thrombophilic polymorphisms, particularly prothrombin G20210A and antithrombin III, rather than any single genetic prothrombotic abnormality, appears to signal an increased thromboembolic risk in patients undergoing total hip arthroplasty. Future refinements and availability of these tests will likely allow preoperative identification of patients with an increased genetic predisposition for thromboembolism.

Arthroplasty, Replacement, Hip↗

PubMed2002

Misremembering pictured objects: people of all ages demonstrate the boundary extension illusion.

In the boundary extension illusion, subjects recollect more of a photographed scene than was originally shown. In this study, first- and fifth-grade children, young adult college students, and older adults studied 4 one-object or 4 two-object picture stimuli for 15 s each. Immediately after each visual scene was shown, the subjects drew it from memory inside a rectangle that was the same size as the previous picture. This study demonstrated that all age groups, from young children to older adults, were susceptible to the boundary extension illusion. This finding is discussed in terms of Intraub's perceptual schema hypothesis and Johnson's source-monitoring hypothesis.

Adolescent↗