Heart failure is a syndrome characterized initially by left ventricular dysfunction that triggers countermeasures aimed to restore cardiac output. These responses are compensatory at first but eventually become part of the disease process itself leading to further worsening cardiac function. Among these responses is the activation of the sympathetic nervous system (SNS) that provides inotropic support to the failing heart increasing stroke volume, and peripheral vasoconstriction to maintain mean arterial perfusion pressure, but eventually accelerates disease progression affecting survival. Activation of SNS has been attributed to withdrawal of normal restraining influences and enhancement of excitatory inputs including changes in: 1) peripheral baroreceptor and chemoreceptor reflexes; 2) chemical mediators that control sympathetic outflow; and 3) central integratory sites. The interface between the sympathetic fibers and the cardiovascular system is formed by the adrenergic receptors (ARs). Dysregulation of cardiac beta(1)-AR signaling and transduction are key features of heart failure progression. In contrast, cardiac beta(2)-ARs and alpha(1)-ARs may function in a compensatory fashion to maintain cardiac inotropy. Adrenergic receptor polymorphisms may have an impact on the adaptive mechanisms, susceptibilities, and pharmacological responses of SNS. The beta-AR blockers and the inhibitors of the renin-angiotensin-aldosterone axis form the mainstay of current medical management of chronic heart failure. Conversely, central sympatholytics have proved harmful, whereas sympathomimetic inotropes are still used in selected patients with hemodynamic instability. This review summarizes the changes in SNS in heart failure and examines how modulation of SNS activity may affect morbidity and mortality from this syndrome.

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A significant proportion of patients undergoing elective abdominal aortic aneurysm repair are susceptible to the development of delirium and are at risk for cognitive dysfunction after surgery. Our findings have implications for promoting long-term lifestyle changes, including smoking cessation and improved management of mental health as risk-reduction strategies.

The authors estimated noninvasively the wall stress distribution for actual abdominal aortic aneurysms (AAAs) in vivo on a patient-to-patient basis and correlated the peak wall stress (PWS) with various geometrical parameters. They studied 39 patients (37 men, mean age 73.7 +/- 8.2 years) with an intact AAA (mean diameter 6.3 +/- 1.7 cm) undergoing preoperative evaluation with spiral computed tomography (CT). Real 3-dimensional AAA geometry was obtained from image processing. Wall stress was determined by using a finite-element analysis. The aorta was considered isotropic with linear material properties and was loaded with a static pressure of 120.0 mm Hg. Various geometrical parameters were used to characterize the AAAs. PWS and each of the geometrical characteristics were correlated by use of Pearson's rank correlation coefficients. PWS varied from 10.2 to 65.8 N/cm2 (mean value 37.1 +/- 9.9 N/cm2). Among the geometrical parameters, the PWS was well correlated with the mean centerline curvature, the maximum centerline curvature, and the maximum centerline torsion of the AAAs. The correlation of PWS with maximum diameter was nonsignificant. Multiple regression analysis revealed that the mean centerline curvature of the AAA was the only significant predictor of PWS and subsequent rupture risk. This noninvasive computational approach showed that geometrical parameters other than the maximum diameter are better indicators of AAA rupture.