During the last years surprising data have been reported showing that the
nitric oxide synthase synthesizes and releases apolipoprotein-B containing lipoproteins (apoB), which are structurally much alike plasma low-density lipoprotein particles [1] and [2]. This phenomenon has been confirmed in several different species including humans. What we know from experiments performed in transgenic animals supported by human data is that myocardial apoB production is probably not important for maintenance of normal cardiac function and structure. Both knock-out mice and humans with the rare genetic defect resulting in inability to express MTP (microsomal transfer protein – initial step in the synthesis of apoB) and consequently in abetalipoproteinemia, have normal cardiac structure and function. Accordingly, the research focus during the last years was oriented toward defining the role of myocardial apoB in the pathophysiological settings. It has been demonstrated that apoB may be involved in cardioprotection by means of elimination of toxic intracellular lipids [3]. While it has been reported that apoB overexpression may prevent or inhibit development of cardiomyopathy due to excessive intracellular lipid accumulation, the importance of this biochemical system for the
heart during acute myocardial infarction (MI) and acute heart failure (HF) has not been studied. The aim of this study was first to determine the time-dependent myocardial apoB synthesis in response to injury caused by ischemia-reperfusion (IR) and in chronic post-MI HF. Second, we sought to determine whether myocardial overexpression of apoB affects myocardial function, cardiac remodelling, ventricular arrhythmias and survival after acute MI. Our data support the hypothesis that myocardial apoB may be a major endogenous protective system in the heart.
