Echocardiographic analysis of dysfunctional and normal myocardial segments before and immediately after coronary artery bypass graft surgery.

Echocardiography has revealed evidence of "subnormal" regional contraction patterns that result from myocardial ischemia and are often accompanied by nonadjacent "hyperkinetic" regions. Whether these regions of hyperkinetic wall motion persist unchanged or revert to normal after coronary artery bypass graft (CABG) surgery has not been studied in humans. Using echocardiography, we evaluated both dysfunctional and normal myocardial regions for changes in segmental wall motion and percent of systolic wall thickening that occurred immediately after CABG surgery in 32 patients. Segmental wall motion analysis before CABG surgery in these patients revealed that 170 (66%) of 256 myocardial segments were subnormal, of which 115 (67%) improved and 102 (60%) returned to normal immediately after CABG surgery. Eleven myocardial segments that were hyperkinetic before CABG surgery returned to normal after CABG surgery. Preoperatively, 162 (63%) of 256 myocardial segments had systolic wall thickening less than 30%, which increased from 11.8% +/- 8.9% to 24.3% +/- 14.3% (mean +/- SD) (P less than 0.01) postoperatively. Conversely, a reverse trend was found when systolic wall thickening was greater than 30% before CABG surgery: thickening decreased from 46.2% +/- 13.8% to 33.4% +/- 14.8% after CABG surgery (P less than 0.01). Thus, we conclude that immediately after CABG surgery, there is a recovery of function in some myocardial segments and a reduction in function in others. Furthermore, we conclude that the semiquantitative assessment of percent of systolic wall thickening is a more reliable (consistent) echocardiographic index of myocardial function compared with the qualitative assessment of segmental wall motion immediately after CABG surgery.     

Recovery from Duret hemorrhage: a rare complication after craniotomy--case report

A 44-year-old female presented with Duret hemorrhage due to transtentorial herniation by extradural hematoma as a complication after craniotomy for treatment of spontaneous middle cranial fossa cerebrospinal fluid leakage through the oval window. Brain computed tomography revealed linear hemorrhage in the midbrain and the rostral pons. She awoke after 2 weeks in a coma, despite showing ocular bobbing and bilateral intranuclear ophthalmoplegia. She was discharged from the hospital with minimal neurological defects. Duret hemorrhage is usually fatal, but this case shows that early surgical decompression is the most important factor to avoid the worst sequelae.     

Hydrogen peroxide inhibits gap junctional intercellular communication in glutathione sufficient but not glutathione deficient cells

Cell to cell communication via gap junctions is essential in the maintenance of the homeostatic balance of multicellular organisms. Aberrant intercellular gap junctional communication (GJIC) has been implicated in tumor promotion, neuropathy and teratogenesis. Oxidative stress has also been implicated in similar pathologies such as cancer. We report a potential link between oxidative stress and GJIC. Hydrogen peroxide, a known tumor promoter, inhibited GJIC in WB-F344 rat liver epithelial cells with an I50 value of 200 microM. Inhibition of GJIC by H2O2 was reversible as indicated by the complete recovery of GJIC with the removal of H2O2 via a change of fresh media. Free radical scavengers, such as t-butyl alcohol, propylgallate, and Trolox, did not prevent the inhibition of GJIC by H2O2, which indicated that the effects of H2O2 on GJIC was probably not a consequence of aqueous free radical damage. The depletion of intracellular GSH reversed the inhibitory effect of H2O2 on GJIC. The treatment of glutathione- sufficient cells with H2O2 resulted in the hyperphosphorylation of connexin43, which is the basic subunit of the hexameric gap junction protein, as determined by Western blot analysis. TPA, a well-known tumor promoter, also inhibits GJIC via hyperphosphorylation of GJIC, which is a result of protein kinase-C activation. However, H2O2 also induced hyperphosphorylation in GSH-deficient cells that had normal rates of GJIC. Therefore, the mechanism of GJIC inhibition must be different from the TPA-pathway and involves GSH.      

Patient's quality of life and hearing outcomes after stapes surgery

Objectives: To determine the quality of life (QOL) after stapes surgery and whether audiological parameters for hearing correlate with specific QOL factors. Design: A retrospective cross‐sectional study. Setting: A tertiary referral centre. Participants: A series of 35 patients who underwent stapes surgery of which three were excluded because they were <18 years of age, chronically or mentally ill, or in a dependant relationship. Response rate was 93% (30/32). Nine were further excluded because they had revision or bilateral surgery, or missing data. Twenty‐one patients were included in this study. Main outcome measures: The Glasgow Benefit Inventory (GBI) was used to evaluate general QOL and the Hearing Disability and Handicap Scale (HDHS) was used as a disease‐specific measure. The Belfast Rule of Thumb and Glasgow Benefit Plot assessed hearing outcomes. Results: Operative success was 86% using the Belfast Rule of Thumb and 95% had closure of the air–bone gap to within 20 dB. 81.8% of patients reported a better overall QOL as surgery. Glasgow Benefit Inventory Social and GBI Physical scores correlated positively with the HDHS speech component (P < 0.05). The duration of hearing loss correlated inversely with the average HDHS score (P < 0.05). Conclusion: The majority of patients report a better QOL as undergoing stapes surgery. Speech impacts on people's physical and social QOL of patients. Quality of life tools, in addition to objective audiologic measurements can provide clinicians with patients’ subjective perspective that helps guide clinical decision‐making and counselling.     

Upfront high-dose sequential therapy (HDS) versus VACOP-B with or without HDS in aggressive non-Hodgkin's lymphoma: long-term results by the NHLCSG.

BACKGROUND: There is not univocal concordance for using high-dose sequential therapy (HDS) as first-line treatment for aggressive non-Hodgkin's lymphoma (NHL). We designed this study to evaluate the usefulness of HDS followed by high-dose therapy (HDT) with autologous stem cell transplantation as front-line treatment in different subsets of aggressive NHL. PATIENTS AND METHODS: Among 223 patients aged 15-60 years with aggressive, advanced stage NHL, 106 patients were randomized to VACOP-B (etoposide, doxorubicin, cyclophosphamide, vincristine, prednisone, bleomycin) for 12 weeks (plus HDS/HDT in case of persistent disease) (arm A), and 117 patients to VACOP-B for 8 weeks plus upfront HDS/HDT (arm B). RESULTS: According to the intention-to-treat analysis, the complete response rate was 75% for arm A and 72.6% for arm B. With a median follow-up of 62 months there was no difference in 7-year probability of survival (60% and 57.8%; P = 0.5), disease-free survival (DFS) (62% and 71%; P = 0.2) and progression-free survival (PFS) (44.9% and 40.9%; P = 0.7) between the two arms. Subgroup analyses confirmed that the best results in terms of survival, DFS and PFS were achieved by patients with large B-cell NHL without bone marrow (BM) involvement, independently of the treatment arm. Results were poorer in other categories of patients and poorest in patients with BM involvement. CONCLUSIONS: Aggressive NHL patients do not benefit from upfront HDS/HDT.     

Spinal fractures in patients with ankylosing spondylitis

The ankylosed spine is prone to fracture even after minor trauma due to its changed biomechanical properties. The two central features of ankylosing spondylitis (AS) that promote the pathological remodeling of the spine are inflammation and new bone formation. AS is also associated with osteoporosis that is attributed to an uncoupling of the bone formation and bone resorption processes. Therefore, bone resorption occurs and promotes weakening of the spine as well as increased risk of vertebral fractures which can be hugely different in terms of clinical relevance. Even in the presence of symptomatic clinical vertebral fractures, the diagnosis can be overruled by attributing the pain to disease activity. Furthermore, given the highly abnormal structure of the spine, vertebral fracture diagnosis can be difficult on the basis of radiography alone. CT can show the fractures in detail. Magnetic resonance imaging is considered the method of choice for the imaging of spinal cord injuries, and a reasonable option for exclusion of occult fractures undetected by CT. Since it is equally important for radiologists and clinicians to have a common knowledge base rather than a compartmentalized view, the aim of this review article was to provide the required clinical knowledge that radiologists need to know and the relevant radiological semiotics that clinicians require in diagnosing clinically significant injury to the ankylosed spine.