The Effect of Left Ventricular Intracavitary Volume on the Unipolar Electrogram

In order to examine the effects of ventricular distention on the unipolar electrogram (UEG), an isolated rabbit heart modified Langendorff preparation was utilized. Left ventricular (LV) volume was adjusted using ionically permeable (PB = 9 hearts) or ionically impermeable balloons (IB = 4 hearts). LV UEGs, LV end-diastolic pressure (EDP), and LV minor axis dimension (MAD), as measured by ultrasonic transducers, were recorded. Three hundred twenty-five eiectrograms were digitized and analyzed with customdesigned software, In the PB group, a significant inverse linear relationship was found between UEG amplitude and changes in MAD (P < 0.0001). For each animal, this relationship had an R value > 0.8 and a P value < 0.0001. There was also a significant inverse linear relationship between UEG slope and changes in MAD (P < 0.01). UEG amplitude and slope also exhibited a significant inverse relationship to changes in LV EDP, which were best described by a third order polynomial function. In the IB group, no significont relationship was found between either UEG amplitude or slope and MAD or EDP. In this study, intracavitary volume exerted a profound and significant influence on UEG amplitude and slope. This effect was due to increases in conductive intraventricular volume and not to myocardial stretch     

Propafenone-Induced Torsade de Pointes: Cross-Reactivity with Quinidine

A 77-year-oid/emale with new onset atrial fibrillation occurring in the absence of structural heart disease developed torsade de pointes during therapy with quinidine bisulfate 500 mg orally every 8 hours. Ten days after quinidine therapy had been discontinued she developed torsade de pointes while receiving propafenone 300 mg orally every 8 hours. This case demonstrates that propafenone may be associated with torsade de pointes and suggests a cross-reactivity between this effect and prior occurrence of torsade de pointes on Class IA antiarrhythmic drug therapy.     

Pingueculae--An Association with Renal Failure

One hundred and forty-four patients who had chronic renal failurewere examined for the presence of pingueculae. A significantlygreater incidence was found between the ages of 20 to 40 inthese patients compared with an age- and sex-matched controlgroup. There was no difference in sex-incidence or between thosetreated with haemodialysis or transplantation. The levels ofcholesterol, triglycerides, calcium, and inorganic phosphatein the plasma were not related to the presence of pingueculae.Detailed structural andchemical analyses of pingueculae aredescribed.     

NSAID-induced antral ulcers are associated with distinct changes in mucosal gene expression

Background  The basis for individual variation in gastroduodenal vulnerability to NSAIDs is not well understood.
Aim  To assess whether a gene expression signature is associated with susceptibility to gastroduodenal ulcerations.
Methods  Twenty-five Helicobacter pylori negative adults were treated for 7 days with naproxen 500 mg b.d. Subjects underwent baseline and post-treatment endoscopy, during which biopsies were taken from antrum and duodenum. RNA extraction and cDNA synthesis were performed, followed by PCR of 23 genes relevant to mucosal injury and repair. Fold changes in gene expression were compared between subjects who developed ulcers and those who did not.
Results  Compared with subjects who did not develop ulcers ( n  = 18), subjects who developed antral ulcers ( n  = 7) had significantly greater mucosal up-regulation of interleukin-8 [Fold change = 33.5 (S.E.M. = 18.5) vs. −7.7 (3.2)] and of cyclo-oxygenase-2 [2.3 (1.7) vs. −10.8 (2.2)]. Conversely, non-ulcer subjects had significantly greater up-regulation of toll-like receptor-4, cyclo-oxygenase-1 and hepatocyte growth factor [14.0 (2.2) vs. −0.8 (1.0), 9.8 (2.4) vs. 0.0 (0.7) and 8.2 (2.6) vs. −2.2 (0.3) respectively].
Conclusions  NSAID-induced antral ulcers are associated with a specific pattern of gastroduodenal mucosal gene expression. These patterns may provide an insight into the molecular basis of individual susceptibility to mucosal injury.