Subclinical atherosclerosis in patients with chronic psoriasis: a potential association.

BACKGROUND: The immunological abnormalities that lead to the development of psoriasis suggest that these patients may be at increased risk for other inflammatory state which may enhance atherosclerosis. OBJECTIVE: To assess the presence of subclinical atherosclerosis in psoriatic patients who haven't associated traditional cardiovascular risk factors, and to correlate these findings with colour Doppler echocardiographic parameters. METHODS: The study included 80 patients with chronic psoriasis together with 50 age and sex matched healthy volunteers served as control group. Patients who had classic cardiovascular risk factors or had cardiovascular or cerebrovascular events were excluded. Carotid artery intima-media thickness (IMT) and carotid plaques were measured in the carotid arteries by using high-resolution B-mode ultrasound. Also, echocardiographic study was performed using ultrasound imaging system in all cases and controls. RESULTS: Patients with psoriasis had increased carotid artery IMT compared with controls (means 0.9 +/- 0.2 mm vs. 0.7 +/- 0.1 mm; P < 0.001). Carotid IMT positively correlated with patients age, duration of the disease and severity of psoriasis. There was no significant difference in echocardiographic parameters in psoriatic patients compared with controls, also no significant correlation between carotid IMT and echocardiographic parameters were observed in psoriatic patients. CONCLUSION: The increased carotid artery IMT in patients with chronic psoriasis suggesting that chronic psoriasis is associated with subclinical atherosclerosis with increased risk of cardiovascular disease. So, dermatologists should advice their patients to avoid traditional cardiovascular risk factors and to routinely checkup to reduce cardiovascular morbidity and mortality.

Beach impacts of shore-parallel breakwaters backing offshore submerged ridges, Western Mediterranean Coast of Egypt.

Seven breakwaters were constructed behind offshore submerged ridges to create a safe area for swimming and recreational activities west of Alexandria on the Mediterranean coast of Egypt. Morphodynamic evaluation was based on the modified Perlin and Dean numerical model (ImSedTran-2D) combined with successive shoreline and beach profile surveys conducted periodically between April 2001 and May 2005. Results reveal insignificant morphologic changes behind the detached breakwaters with slight coastline changes at the down and up-drift beaches of the examined breakwaters (+/-10 m). These changes are associated with salient accretion (20-7 0m) in the low-energy leeside of such structures. Concurrent with this sand accretion is the accumulation of a large amount of benthic algae (Sargassum) in the coastal water of the shadow area of these structures, which in turn have adverse effects on swimmers. Practical measures proposed in this study have successfully helped in mitigating such accumulation of algae in the recreation leeside of the breakwaters. The accumulation of Sargassum, together with the virtual insignificant changes in the up-drift and down-drifts of these structures, is a direct response to both coastal processes and the submerged carbonate ridges. Coastal processes encompass reversal of the directions of long-shore sand transport versus shoreline orientation, the small littoral drift rate and sand deficiency of the littoral zone. The beach response to the breakwaters together with the submerged ridges has also been confirmed by applying the ImSedTran-2D model. Results indicate that submerged ridges play a principal role in the evolution of beach morphology along the west coast of Alexandria. Although the study area is exposed to more than 70% wave exposures, the morphodynamic behavior of the beaches indicates that the submerged ridges act in a similar way as an additional natural barrier together with the artificial detached structures.

Effects of uremic serum on isolated cardiac myocyte calcium cycling and contractile function.

BACKGROUND: Diastolic dysfunction occurs in patients with chronic renal failure. Moreover, serum from uremic patients contains one or more inhibitors of the plasmalemmal Na,K-ATPase (sodium pump). We hypothesized that a circulating substance present in uremic sera contributes to both sodium pump inhibition and diastolic dysfunction. METHODS: Serum samples were obtained from six patients with chronic renal failure and diastolic dysfunction. RESULTS: Their serum samples caused marked inhibition of Na,K-ATPase purified from dog kidney at all concentrations studied (all P < 0.01) and also impaired ouabain-sensitive rubidium uptake by myocytes isolated from Sprague-Dawley rats (P < 0.01). These cardiac myocytes were studied for their contractile function with video-edge detection and calcium metabolism with indo-1 fluorescence spectroscopy after exposure to these uremic sera. These uremic sera caused increases in myocyte fractional shortening (P < 0.01) as well as an increase in the time constant of relengthening (P < 0.01). Examining the calcium transient, the time constant for calcium recovery was also increased (P < 0.01). Exposure of these cells to sera from age- and sex-matched healthy subjects did not result in significant changes in contraction or calcium cycling. Extracts of uremic serum samples inhibited isolated Na,K-ATPase whereas extracts of normal serum samples did not. The effect of uremic serum extracts on contractile function and calcium cycling were quite similar to that of intact serum or the addition of ouabain. Co-incubation of uremic serum extract with an antibody fragment directed against digoxin markedly attenuated the inhibition of Na,K-ATPase activity and completely prevented any effects on calcium cycling or contractile function. CONCLUSION: These data show that one or more substances are present in uremic sera that acutely cause increased force of contraction and impaired recovery of cardiac myocyte calcium concentration as well as impaired relaxation. As these effects are similar to that seen with ouabain and can be prevented by co-incubation with an antibody fragment to digitalis, which also attenuates the sodium pump inhibitory effect, we suggest that this (these) substance(s) circulating in uremic sera and inhibiting the sodium pump also causes the acute diastolic dysfunction seen in our system.