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1.  Right ventricular remodeling in restrictive ventricular septal defect 
Restrictive ventricular septal defect (rVSD) presents with little/no hemodynamic aberrations despite a patent septal defect. Clinically, these patients are observed with the hope that the defect will functionally close over time without the need for surgical repair and development of heart failure. Without evidence supporting a definitive therapeutic strategy, rVSD patients may have increased risk of a poor outcome. We tested the hypothesis that rVSD results in subclinical RV diastolic dysfunction and molecular remodeling. Five pigs underwent surgical rVSD creation. Echocardiography, hemodynamics, myocyte contractility experiments, and proteomics/Western blot were performed 6-weeks post-rVSD and in controls. *p < 0.05. LV and RV hemodynamics in rVSD were comparable to controls. The tricuspid valve early/late diastolic inflow velocity ratio (TV E/A ratio) decreased from 1.6 ± 0.05 in controls to 1.0 ± 0.08* in rVSD, indicating RV diastolic dysfunction. rVSD RV myocytes showed abnormalities in contraction (departure velocity (Vd) − 51%*, Vd time +55%*) and relaxation (return velocity (Vr) −50%*, Vr time +62%*). Mitochondrial proteins (fatty acid, TCA cycle) increased 2-fold*, indicating heightened RV work. Desmin protein upregulated 285%* in rVSD RV myocardium, suggesting cytoskeletal remodeling. rVSD causes RV diastolic dysfunction, myocyte functional impairment, and mitochondrial/cytoskeletal protein upregulation in our model. Desmin upregulation may hinder sarcomeric organization/relaxation, representing a key subclinical early marker for future RV dysfunction. TV E/A measurements are a non-invasive modality to assess rVSD patients for diastolic dysfunction. Translational research applications may lead to fundamental changes in the clinical management of rVSD by providing evidence for early repair of the defect.
PMCID: PMC4263504  PMID: 20637777
Ventricular septal defect; Diastolic dysfunction; Desmin; Remodeling; Congenital; Cytoskeleton; Echocardiography
2.  Uvular Edema Secondary to Snoring Under Deep Sedation 
Anesthesia Progress  2006;53(1):13-16.
A 57-year-old male with a documented history of obstructive sleep apnea with loud snoring received deep intravenous sedation with midazolam, fentanyl, ketamine, and propofol infusion and a left interscalene brachial plexus nerve block for a left biceps tendon repair. Loud snoring during the case was noted. On the second postoperative day, he was observed to have significant uvular edema. After due consideration of the various elements in the differential diagnosis, it was concluded that negative pressure trauma from deep snoring during the sedation was the most likely etiology.
PMCID: PMC1586864  PMID: 16722279
Uvular edema; Obstructive sleep apnea; Deep sedation; Negative pressure edema

Results 1-2 (2)