Echocardiography was performed simultaneously with LVEDP measurements. Both, E/Ea and E/(EaxSa) were calculated, using the average of the velocities of the septal and lateral mitral annulus.\n\nResults:

A significant linear correlation was demonstrated between E/(EaxSa) and LVEDP (r = 0.81, p <0.001); this was superior to E/Ea (r = 0.73, p <0.001), Sa (r = -0.59, p = 0.004), pulmonary artery systolic pressure (r = 0.57, p = 0.007), E-wave (r = 0.45, p = 0.009), Ea (r = -0.31, p = 0.01), and left atrial volume (r = 0.28, p = 0.02). No significant relationships could be demonstrated between LVEDP and the LV ejection fraction. The area under the receiver-operating characteristic (ROC) curve for prediction of LVEDP >15 mmHg was greatest for E/(EaxSa) (AUC = 0.87, p <0.001), followed by the E/Ea ratio (AUC = 0.81, p <0.001). A statistical comparison of the ROC curves indicated that E/(EaxSa) was Ion Channel Ligand Library clinical trial more accurate than E/Ea (p = 0.02). The optimal E/(EaxSa) cut-off to predict a LVEDP >15 Veliparib mmHg was 1.95 (85% sensitivity, 83% specificity).\n\nConclusion: E/(EaxSa) correlates strongly with LVEDP, and can serve as a simple and accurate echocardiographic index for the estimation of LVEDP in patients with severe MR.”
“BACKGROUND: Exposure to particulate

matter smaller than = 2.5 mu m in diameter (PM2.5) increases blood pressure (BP) in humans and animal models. Abnormal activation of the sympathetic nervous system may have a role in the acute BP response to PM2.5 exposure. The mechanisms responsible for sympathetic nervous system activation and its role in chronic sustenance of hypertension in response to PM2.5 exposure are currently unknown. OBJECTIVES: We investigated whether

central nervous system inflammation may be implicated in chronic PM2.5 exposure-induced increases in BP and sympathetic nervous system activation. METHODS: C57BL/6J mice were exposed to concentrated ambient PM2.5 (CAPs) for 6 months, and we analyzed BP using radioactive telemetric transmitters. We assessed sympathetic tone by measuring low-frequency BP variability (LF-BPV) and urinary norepinephrine excretion. We also tested the selleck kinase inhibitor effects of acute pharmacologic inhibitors of the sympathetic nervous system and parasympathetic nervous system. RESULTS: Long-term CAPs exposure significantly increased basal BP, paralleled by increases in LF-BPV and urinary norepinephrine excretion. The increased basal BP was attenuated by the centrally acting alpha(2a) agonist guanfacine, suggesting a role of increased sympathetic tone in CAPs exposure-induced hypertension. The increase in sympathetic tone was accompanied by an inflammatory response in the arcuate nucleus of the hypothalamus, evidenced by increased expression of pro-inflammatory genes and inhibitor kappaB kinase (IKK)/nuclear factor-kappaB (NF-kappa B) pathway activation.