I am interested in knowing the ways of high levels of dysfunctional HDL in the acute phase of myocardial infarction induce minor flow-mediated dilation and nitric oxide production and the strategies that have been used do elucidated it.
What are the possible explanations by which HDL dysfunctional causes lower flow-mediated dilation and reduces production of nitric oxide in the setting of acute myocardial infarction?