Implications lor Therapy

Despite strong evidence for the prognostic value ofthe newer markers, such as BNP and CRP, their integration into clinical practice has not become widespread. The primary determinant ofthis pace ofintegration has been the absence of guidance regarding the appropriate therapeutic response. Although therapies that mitigate the risk of an elevated level of troponin in patients with suspected ACS are well defined, to date there is not a consistent base of evidence to guide treatment in response to elevated levels of BNP or CRP.

An intense effort is under way to identify therapies directed at the inflammation underlying plaque instability in patients with ACS. Laboratory and clinical studies have revealed anti-inflammatory effects of established treatments aimed at other contributors to athero-thrombosis (e.g., aspirin, statins, angiotensin-converting enzyme inhibitors and clopidogrel) (43). The evidence for anti-inflammatory actions of statins continues to grow and supports intensive statin therapy as being particularly important for patients with evidence of inflammation (44). In addition, clopidogrel decreases the expression of CD40L and may have a greater impact on reducing ischemic events after percutaneous coronary intervention in patients with elevated markers of inflammation (45). Agonists of the protein peroxisome proliferator activated receptor-a (PPAR-a), such as fibric acid derivatives, can

BNP/NTproBNP, ANP

Fig. 11. Conceptual application of multimarker approach to characterization of patient with ACS. ANP, atrial natriuretic peptide; GP, glycoprotein; IMA, ischemia-modified albumin; MMP, metallo-proteinases; PAI-1, plasminogen activator inhibitor-1; vWF, von Willebrand factor. (Adapted from ref. 2.)

BNP/NTproBNP, ANP

Fig. 11. Conceptual application of multimarker approach to characterization of patient with ACS. ANP, atrial natriuretic peptide; GP, glycoprotein; IMA, ischemia-modified albumin; MMP, metallo-proteinases; PAI-1, plasminogen activator inhibitor-1; vWF, von Willebrand factor. (Adapted from ref. 2.)

reduce the expression of adhesion molecules on vascular endothelial cells, inhibit T-lym-phocyte function, improve vascular reactivity, and reduce production of the potent procoagulant tissue factor. Likewise, the family ofinsulin-sensitizing thiazolidinediones, which act through PPAR-y, are now appreciated to exert anti-inflammatory actions and reduce CRP as well as other inflammatory mediators in patients with diabetes (9). These and other treatments may eventually prove to be useful in modifying the risk associated with elevated levels of markers of inflammation.

Similar investigation targeted at reducing the risk associated with increased concentrations of natriuretic peptides is not as far advanced. Since BNP levels are associated with LV dysfunction as well as the extent of coronary artery disease, it is reasonable to hypothesize that early invasive evaluation and revascularization will reduce the risk linked to higher levels of BNP. However, the available data addressing this hypothesis have been conflicting (see Chapter 24) (18). It is also plausible that agents with favorable long-term effects on LV performance in patients with ischemic heart disease may prove beneficial in this population. At this point, natriuretic peptides may be used to identify patients at increased absolute risk of death and heart failure who have the most to gain from treatments that modify the risk of these events. However, additional research is necessary to test the success of specific interventions for patients with increased levels of BNP.

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