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s 279 placebo for 2 years. Total cholesterol (TC), LDL-C, nonHDL-cholesterol, HDL-cholesterol, VLDL-cholesterol, triglycerides, apolipoprotein A, apolipoprotein B, high-sensitivity C-reactive protein (hs-CRP), and SAAwere measured at 1 and 2 years. Student’s t-tests comparing O3FA versus placebo were used to analyze the change in each lipid parameter at each time point. Results: There were no significant differences in any baseline characteristic between groups (supplement vs. placebo), indicating appropriate randomization. The mean age of subjects was 55 6 10 years, and 53% were women. The mean waist circumference was 110 6 14 cm, median TGs were 157 mg/dL, mean HDL-C was 45 6 13 mg/dL, mean glucose was 103 6 8mg/dL, mean systolic BP was 132 6 13 mmHg, and mean diastolic BP was 83 6 9 mmHg. There were no significant differences (supplement vs. placebo) in TC, LDL-C, non-HDL-C, or HDL-C at year 1 or 2 from baseline. Change in TGs at year 1 from baseline was 37.3 mg/dL lower in the intervention group (P 5 .015) and 30.4 mg/dL lower at year 2 from baseline in the intervention group (P 5 .09). Change in VLDL-C from baseline was 7.41 mg/dL lower at year 1 (P 5 .016) and 6.11 mg/dL lower at year 2 in the intervention group (P 5 .08). There were no significant differences in apoA1 at year 1, but at year 2 the change in apoA1 from baseline was 9.7 mg/dL lower in the intervention group (0.013). Change in apoB at year 1 from baseline was 7.83 mg/dL lower in the intervention group (P 5 .034) and 8.16 mg/dL lower (P 5 .037) at 2 years. There were no significant differences in change in hs-CRP or SAA at year 1 or 2 comparing intervention with placebo. Conclusions: O3FA supplementation in the form of EPA and DHA improves the atherogenic dyslipidemia of MetS by decreasing TGs, VLDL-C and apolipoprotein B in subjects with MetS. Supplementation does not, however, improve inflammatory markers.

A patient in whom the right ureter was inadvertently catheterized at the time of cystometry is described. Upon filling, the patient immediately developed severe colicky right flank pain and the vesical pressure of 150 cmH(2)O triggered the pump's automatic shut-off mechanism. Cystoscopy was performed and confirmed the inadvertent placement of the microtip catheter in the right ureteral orifice. After the catheter was repositioned, symptoms resolved and the remainder of the examination was performed routinely, with normal vesical and urethral pressures.

The objective of this study was to report the frequency of disulfiram-related elevations of four commonly used hepatic screening chemistries using a retrospective record review design. An inpatient alcoholism program was selected for the setting. Patients who had initial laboratory values within the normal range started daily supervised doses of disulfiram, then underwent follow-up testing after 2 and 4 weeks on the drug. The study population consisted of 108 patients receiving disulfiram and 27 patients who did not receive disulfiram (controls). The four screening serum chemistries performed were aspartate aminotransferase (SGOT), alanine aminotransferase (SGPT), alkaline phosphatase, and gamma-glutamyl transferase. Twenty-seven (25%) of the 108 patients who were taking 250 mg of disulfiram a day for 2 to 4 weeks had disulfiram-related elevations in alanine aminotransferase above the upper limit of normal, as opposed to one elevation in 27 patients (4%) for whom disulfiram was not prescribed. In the 108 patients (with initially normal serum chemistries) who were prescribed disulfiram, 32 were discontinued from the drug at 2 weeks and an additional 11 were discontinued from the drug at 4 weeks because of one or more abnormal serum chemistries. Alanine aminotransferase was the most specific and sensitive indicator of the four screening chemistries performed.

Echocardiography is recommended for the detection of valvular regurgitation in asymptomatic users of anorexigens with a heart murmur. To determine the prevalence and diagnostic value of heart murmurs for valvular regurgitation, 223 patients receiving dexfenfluramine therapy for 6.9 months and 189 matched controls underwent history and cardiac auscultation by experienced noncardiologists unaware of echocardiography. Color Doppler echocardiograms were interpreted by 3 observers unaware of patients' clinical data. The frequency of at least mild regurgitation of any valve and abnormal regurgitation (moderate mitral or tricuspid or mild aortic regurgitation) were determined. Heart murmurs heard in 31 dexfenfluramine users (14%) and in 20 controls (11%) were all systolic and of grade I to II/VI intensity. Mild or worse regurgitation of any valve showed a trend in patients (18% vs 11.6% in controls, odds ratio [OR] 1.66, confidence interval [CI] 0.95 to 2.9, p = 0.08), but abnormal regurgitation (includes Food and Drug Administration grade regurgitation) was more common in patients (9% vs 3% in controls, OR 3.0, CI 1.18 to 7.65, p = 0.02). In dexfenfluramine users, heart murmurs were associated with at least mild or abnormal regurgitation (OR 3.1 and 3.05, 95% CI 1.34 to 7.13 and 1.1 to 8.67; p = 0.008 and 0.036, respectively), had a specificity of 89% and 88%, negative predictive value of 85% and 93%, but sensitivity of 37% and 30%, and positive predictive value of 35% and 19%, respectively. Most valves missed by cardiac auscultation had normal morphology and mild regurgitation. Finally, heart murmurs had better diagnostic value for either type of valvular regurgitation than heart murmurs and clinical variables or clinical variables alone. In summary, in dexfenfluramine users the prevalence of heart murmurs was low and their absence predicted absence of mild or worse regurgitation of any valve or abnormal valvular regurgitation. Therefore, cardiac auscultation should be the screening method of choice for detecting valvular regurgitation in users of anorexigens.

Hypertension occurs commonly and early in the natural history of autosomal dominant polycystic kidney disease (ADPKD), affecting both renal and patient outcome. Activation of the renin angiotensin aldosterone system due to cyst expansion and local renal ischaemia plays an important role in the development of ADPKD related hypertension and left ventricular hypertrophy (LVH), a known important risk factor for cardiovascular morbidity and mortality. The aim of this study was to investigate the effects of an angiotensin converting enzyme (ACE) inhibitor, enalapril, on renal function, blood pressure and LVH in hypertensive ADPKD patients.Fourteen hypertensive ADPKD patients (11 men, 3 women; mean age: 40 years) were included in the study. All patients had LVH and creatinine clearance (Cer) greater than 50 ml/min/1.73 m2. The patients were followed for 7 years on enalapril therapy. The effects of enalapril on renal function, blood pressure and LVH were investigated.Baseline measurements of mean arterial pressure (MAP), Ccr and left ventricular mass index (LVMI) were 110 +/- 2 mmHg, 84 +/- 6 ml/min/1.73 m2 and 146 +/- 4 g/m2, respectively. After one year of enalapril therapy there was a significant decrease in MAP (94 +/- 3 mmHg, P0.005) which remained stable until the end of the study at 7 years (94 +/- 1 mmHg, P0.005 vs baseline). There was also a significant decrease in LVMI (131 +/- 6 g/m2, P0.05) after year 1 which continued to decrease until the end of the study reaching 98 +/- 6 g/m2 (P0.01 vs year 1 and baseline). Although Ccr remained stable after year 1, a significant decrease was observed after 7 years of follow-up (59 +/- 6 ml/min, P0.001 vs year 1 and baseline).ACE inhibition in hypertensive ADPKD patients provided long-term reversal of LVH in association with a mean 3.6 ml/min/year decline of Ccr. These preliminary results have potential important implications for cardiovascular and renal protection in ADPKD.

We and others have previously shown that carvedilol improves left ventricular (LV) function and symptoms in chronic heart failure. This improvement in LV function has also been shown to be associated with an improvement in survival. This study evaluates the effect of carvedilol on LV mass, geometry, and degree of mitral regurgitation (MR). In 59 patients with symptomatic heart failure and LV ejection fraction

Pelvic organ prolapse is usually caused by weakness of the pelvic diaphragm. Descent of the pelvic diaphragm places stress on the endopelvic connective tissue support system. Subsequent increases in intra-abdominal pressure result in prolapse. In the majority of cases, labor and childbirth are thought to be the primary factors responsible for pelvic neuropathies and tissue damage that predispose to the development of POP. Certain connective tissue defects, congenital defects, and operative procedures also contribute to pelvic support defects.

Enzymes and other factors secreted by degranulating neutrophils (polymorphonuclear leukocytes, PMNs) mediate endothelial injury, thrombosis, and vascular remodeling. In bacteremia and sepsis syndrome and their consequent complications (including acute respiratory distress syndrome and systemic ischemia-reperfusion resulting from septic shock), neutrophil degranulation is an important mechanism of injury. In related studies, we found that human endothelial cells regulate neutrophil degranulation and that inflammatory cytokines induce synthesis of degranulating factors by human endothelial cells. Here we show that lipopolysaccharides (LPS) from gram-negative bacteria were the most potent agonists for release of degranulating activity by endothelial cells when compared to several cytokines and stimulatory factors. LPS also induced the release of degranulating signals for PMNs from a human endothelial cell line, EA.hy 926. Interleukin 8 (IL-8) is synthesized by endothelial and EA.hy 926 cells in response to LPS and induces neutrophil degranulation. However, complementary strategies using receptor desensitization, translation of messenger RNA by Xenopus laevis oocytes, and purification and analysis of factors from conditioned supernatants demonstrated that degranulating factors distinct from IL8 are generated in response to LPS. The characteristics of a partially purified degranulating factor isolated from conditioned supernatants distinguished it from known chemokines and other factors that induce PMN degranulation and are generated by endothelial cells in response to LPS. Thus, cultured human endothelial cells and endothelial cell lines synthesize several unique signaling molecules that can trigger neutrophil granular secretion. If produced in vivo in response to LPS or other pathologic agonists, these degranulating signals may activate PMNs in combination or in sequence, initiating or propagating vascular damage.

We examined the utility of three-dimensional (3D) reconstruction of two-dimensional color Doppler images of the proximal jet to quantify the effective area of an orifice in an in vitro model. Steady and pulsatile flows were directed through various orifices; orifice vena contracta areas were quantified with laser flow visualization, thus providing gold standard effective orifice areas. Three-dimensional areas followed vena contracta areas well, although variations in color Doppler gain and 3D gray levels for thresholding produced significant changes in reconstructed images. These variations were minimized by using minimum color gain and 50% gray level threshold. At these settings, 3D areas still overestimated vena contracta areas by approximately 25% because of the poor lateral resolution of the color Doppler system, which caused bleeding of the flow signal past the edges of the proximal jet. Nevertheless, 3D flow images provided a superior format for qualitative and quantitative appreciation of proximal jet shape and dimensions. (J Am Soc Echocardiogr 1998;11:313-21.)

Noninvasive cardiac imaging techniques now make it possible to determine the morphologic and hemodynamic status of patients with aortic stenosis, even in early asymptomatic stages of the disease. This is particularly important since the prognosis is generally poor once symptoms are apparent and since replacement of the aortic valve is usually the only recourse when stenosis is severe.

Background Polymorphonuclear leukocytes, particularly neutrophils, are important mediators of ischemia/reperfusion–induced myocardial and coronary vascular injury. The selectin family of glycoprotein receptors mediates neutrophil “rolling,” a loose, transient adhesion to the coronary endothelium that precedes the firmer adhesion associated with cardiovascular injury. The oligosaccharide sialyl-Lewis x (SLe x ) is the probable neutrophil counterligand for endothelial E- and P-selectin. Administration of analogues of SLe x could potentially prevent neutrophil rolling by competing for the selectin-adhesion sites. We investigated the effects of treatment with an analogue of SLe x in a chronic canine model of ischemia/reperfusion. Methods and Results Anesthetized mongrel dogs were subjected to 90 minutes of ischemia through occlusion of the left anterior descending coronary artery and 48 hours of reperfusion. Five minutes before the onset of reperfusion, dogs received either the SLe x analogue CY-1503 at a dose of 20 mg/kg or normal saline. Myocardial infarct size was measured through triphenyltetrazolium chloride staining, and polymorphonuclear leukocyte accumulation was evaluated through measurement of cardiac myeloperoxidase activity. After adjustment for blood flow, the mean infarct size of control dogs (44.7±4.2%) was not different from that of treated dogs (33.4±4.0%, P =.06), although there was a trend toward a slightly lower value in the treated dogs. Myeloperoxidase activity was not different in the infarcted myocardium of the treated group compared with that of the control group (2.7±0.71 treated versus 1.08±0.41 units/mg protein control, P =.06). Conclusions We conclude that CY-1503 does not substantially or consistently reduce myocardial infarct size or neutrophil accumulation in dogs subjected to ischemia followed by a prolonged period (48 hours) of reperfusion.

This paper reports the final experimental results and conclusions on the performance of an interferometric acousto-optic receiver (IAOR). The receiver is designed to acousto-optically channelize a 1 GHz RF bandwidth spectrum into 128 frequency bins, and generate digital frequency, pulse amplitude, pulse width and TOA words. Experimental results show that the predicted performance improvement over the power acousto-optic receiver (PAOR) is significantly below expectation. Key factors contributing to performance degradation are discussed along with supporting experimental data. Recommendations for further acousto-optic receiver work are presented.© (1991) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

Background In order to establish a consistent method for brachial artery reactivity assessment, we analyzed commonly used approaches to the test and their effects on the magnitude and time-course of flow mediated dilation (FMD), and on test variability and repeatability. As a popular and noninvasive assessment of endothelial function, several different approaches have been employed to measure brachial artery reactivity with B-mode ultrasound. Despite some efforts, there remains a lack of defined normal values and large variability in measurement technique. Methods Twenty-six healthy volunteers underwent repeated brachial artery diameter measurements by B-mode ultrasound. Following baseline diameter recordings we assessed endothelium-dependent flow mediated dilation by inflating a blood pressure cuff either on the upper arm (proximal) or on the forearm (distal). Results Thirty-seven measures were performed using proximal occlusion and 25 with distal occlusion. Following proximal occlusion relative to distal occlusion, FMD was larger (16.2 ± 1.2% vs. 7.3 ± 0.9%, p < 0.0001) and elongated (107.2 s vs. 67.8 s, p = 0.0001). Measurement of the test repeatability showed that differences between the repeated measures were greater on average when the measurements were done using the proximal method as compared to the distal method (2.4%; 95% CI 0.5–4.3; p = 0.013). Conclusion These findings suggest that forearm compression holds statistical advantages over upper arm compression. Added to documented physiological and practical reasons, we propose that future studies should use forearm compression in the assessment of endothelial function.

A 28 year old white woman with no medical history presented to the emergency room with symptomatic non-sustained ventricular tachycardia. She was asymptomatic up to a few days before presentation. Her physical examination was essentially normal and hence did not help with the differential diagnosis of the problem. Bronchoscopic transbronchial biopsy led to the final diagnosis of cardiac sarcoidosis.

In 1925, Dr. Carl J. Wiggers demonstrated that pacing from the canine left ventricle (LV) improved acute hemodynamics [(1)][1]. The advent of pacing catheters delivered by the coronary sinus allowed practical use and exploration of LV or biventricular (BiV) pacing for improving heart failure (HF)

Women with signs and symptoms of ischemia and no obstructive coronary artery disease (CAD) often have microvascular coronary dysfunction (MCD). This has been associated with adverse outcomes including hospitalization for heart failure with preserved ejection fraction (EF). We sought to explore how