从指南看心衰进展课件.ppt

. * * 重点说明：一氧化氮、缓激肽和前列腺素为局部扩血管因子而非体循环作用。 * * Physiologic effects of the renin-angiotensin aldosterone system (RAAS) and other vasoconstor systems is to increase vascular resistance and afterload. Activation of these systems also produce salt and water retention, elevating filling pressures. Angiotensin II acts on the AT1 receptor to cause vasoconstriction, sodium retention and other physiologic effects. Interventions have been developed to prevent decompensated heart failure by blocking the the renin angiotensin system and sympathetic nervous system (e.g. ACE inhibitors and beta blockers). Activation of the natriuretic peptide system is beneficial in heart failure. ANP and BNP cause vasodilation and sodium excretion. In decompensated heart failure patients this system is overwhelmed. Interventions have now been developed that act on the natriuretic peptide system to augment（增加） its actions using pharmacologic dosing of B-type natriuretic peptide (BNP). The use of this therapy can restore the balance of these competing systems and be used to reverse acute decompensated heart failure. As demonstrated here, patients with acutely destabilized heart failure had significantly higher values for NT-proBNP, compared to those with chronic stable heart failure or those without incident or prevalent heart failure at the time of enrollment. Examining patients as a function of heart failure symptom severity, we also see that NT-proBNP concentrations are higher in those with more severe symptoms, although a significant degree of overlap between groups is noted. In contrast to an age-independent rule out cut-point, the ICON investigators found that age stratification of the ‘rule in’ cut-point for NT-proBNP yielded superior accuracy compared to a single age independent cut-point. By age stratifying, sensitivity is preserved, while specificity is improved in elders, resulting in a significant rise in positive predictive value, and a shrinking of the number of “grey zone” resu