Secondly, mirroring the clinical finding showing a positive association between anti-apoA-1 IgG levels and resting heart rate [26], a well-established cardiovascular prognostic feature after MI [27–29], in vitro studies demonstrated that in presence of aldosterone, anti-apoA-1 IgG can elicit a dose-dependent increase of the spontaneous contraction rate of neonatal rat ventricular cardiomyocytes [26, 49]. This evidence concerns the gene APOA1 and myocardial infarction.