Does the Magnitude of the Electrocardiogram QT Interval Dispersion Predict Stroke Outcome?

BACKGROUND: QT dispersion, maximal interlead difference in QT interval on 12-lead electrocardiogram (ECG), measures cardiac repolarization abnormalities. Data are conflicting whether QT dispersion predicts adverse outcome in acute ischemic stroke (AIS) patients. Our objective is to determine if QT dispersion predicts: (1) short-term clinical outcome in AIS, and (2) stroke location (insular versus noninsular cortex). METHODS: Admission ECGs from 412 consecutive patients with acute stroke symptoms from 2 university-based stroke centers were reviewed. QT dispersion was measured. A neuroradiologist reviewed brain imaging for insular cortex involvement. Favorable clinical outcomes at discharge were modified Rankin Scale (mRS) score of 0-1, discharge National Institutes of Health Stroke Scale (NIHSS) score less than 2, and discharge to home. Multiple logistic regressions were performed for each outcome measure and to determine the association between insular infarct and QT dispersion. RESULTS: Of 145 subjects in the final analysis, median age was 65 years (interquartile range [IQR] 56-75), male patients were 38%, black patients were 68%, median QT dispersion was 78 milliseconds (IQR 59-98), and median admission NIHSS score was 4 (IQR 2-6). QT dispersion did not predict short-term clinical outcome for mRS score (odds ratio [OR] = 1.001, 95% confidence interval [CI] .99-1.01, P = .85), NIHSS at discharge (OR = .994, 95% CI .98-1.01, P = .30), or discharge disposition (OR = 1.001, 95% CI .99-1.01, P = .81). Insular cortex involvement did not correlate with QT dispersion magnitude (OR = 1.009, 95% CI .99-1.02, P = .45). CONCLUSIONS: We could not demonstrate that QT dispersion is useful in predicting short-term clinical outcome at discharge in AIS. Further, the magnitude of QT dispersion did not predict insular cortical stroke location.

Enhanced vascularization and survival of neural transplants with ex vivo angiogenic gene transfer.

Restoration of brain function by neural transplants is largely dependent upon the survival of donor neurons. Unfortunately, in both rodent models and human patients with Parkinson's disease the survival rate of transplanted neurons has been poor. We have employed a strategy to increase the availability of nutrients to the transplant by increasing the rate at which blood vessels are formed. Replication-deficient HSV-1 vectors containing the cDNA for human vascular endothelial growth factor (HSVhvegf) and the bacterial beta-galactosidase gene (HSVlac) have been transduced in parallel into nonadherent neuronal aggregate cultures made of cells from embryonic day 15 rat mesencephalon. Gene expression from HSVlac was confirmed in fixed preparations by staining with X-gal. VEGF expression as determined by sandwich ELISA assay of culture supernatant was up to 322-fold higher in HSVhvegf-infected than HSVlac-infected sister cultures. This peptide was also biologically active, inducing endothelial cell proliferation in vitro. Adult Sprague-Dawley rats received bilateral transplants into the striatum, with HSVlac on one side and HSVhvegf on the other. At defined intervals up to 8 weeks, animals were sacrificed and vibratome sections of the striatum were assessed for various parameters of cell survival and vascularization. Results demonstrate dose-dependent increases in blood vessel density within transplants transduced with HSVhvegf. These transplants were vascularized at a faster rate up to 4 weeks after transplantation. After 8 weeks, the average size of the HSVhvegf-infected transplants was twice that of controls. In particular, the survival of transplanted dopaminergic neurons increased 3.9-fold. Taken together these experiments provide convincing evidence that the rate of vascularization may be a major determinant of neuronal survival that can be manipulated by VEGF gene transduction.

Hemorrhagic angiomyolipoma and tuberous sclerosis complex: a case report.

Tuberous sclerosis was first described in 1862 by von Recklinghausen. Since then there have been many advances in our understanding of the diagnosis, pathogenesis, and treatment of this disease complex, especially after it was characterized genetically. While many patients who have tuberous sclerosis present with the classic triad of mental retardation, seizures, and facial "adenoma sebaceum," most do not because of its variable penetrance. The diagnostic criteria have been revised to include patients with tuberous sclerosis who do not match the classic pattern. Here we describe a 44-year-old female without a prior diagnosis who did not have the classic triad but who presented with flank pain. Hemorrhagic angiomyolipoma was diagnosed by computerized tomography scan and she was treated by an embolization procedure. We review tuberous sclerosis and underscore the need to consider this diagnosis for the following reasons: 1. it is not uncommon (slightly more than one in 6,000 live births); 2. its presentation is protean; 3. once the diagnosis is made, search can be made for associated findings that may lead to additional morbidity if not carefully managed, e.g., if an angio-myolipoma is diagnosed, it can be followed and possibly treated; and 4. owing to its autosomal dominant pattern of inheritance, members of the family can be screened appropriately.