Introduction: The current use of lipid lowering therapies and the eligibility for proprotein convertase subtilisin/kexin-9 (PCSK9) inhibitors of patients surviving a myocardial infarction (MI) is poorly known.
Methods: Using the data from two contemporary, nationwide, prospective, real-world registries of patients with stable coronary artery disease, we sought to describe the lipid lowering therapies prescribed by cardiologists in patients with a prior MI and the resulting eligibility for PCSK9 inhibitors according to the European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS) and the Italian regulatory agency (Agenzia Italiana del Farmaco; AIFA) criteria. The study cohort was stratified according to the following low-density lipoprotein cholesterol (LDL-C) levels at the time of enrolment: <70 mg/dl; 70-99 mg/dl and ≥100 mg/dl.
Background: Previous studies have shown that metabolic syndrome (MS) is associated with an increased susceptibility to develop cardiovascular damage (CD). Experimental evidence indicates that inflammation and fibrosis could play a critical role in the development of CD in hypertension. This issue has not been clarified yet in patients with MS.
View Article and Find Full Text PDFObjectives: The metabolic syndrome (MS) is associated with left ventricular hypertrophy (LVH). Previous evidence has shown that LVH is favoured by low levels of atrial natriuretic peptide (ANP), independently from blood pressure (BP), in hypertension. Although levels of natriuretic peptides are known to be lower in obesity, plasma ANP levels have not yet been assessed in MS.
View Article and Find Full Text PDFObjectives: The goal of our study was to investigate the relationships between atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and type A natriuretic peptide receptor (NPRA) gene polymorphisms and left ventricular structure in human essential hypertension.
Background: Experimental evidence supports a key role for natriuretic peptides in the modulation of cardiac mass. This relationship has not yet been described in human disease.
Background: Vasoconstrictive, proliferative and oxidative effects of angiotensin II (Ang II) are mediated by Ang II type 1 (AT1) receptors. The effects of Ang II via the Ang II type 2 (AT2) receptor subtype (AT2R) are less well defined. Growing evidence shows the existence of cross-talk between the Ang II receptor subtypes, which is revealed by AT1R blockade.
View Article and Find Full Text PDFTo investigate the functional relevance of a regulatory mutation affecting the enhancer element PEA2 of the rat ANP gene we transfected rat cardiomyocytes and aortic endothelial cells with either the mutant or the wild-type ANP promoter construct (-683 +54) and performed CAT assays both at baseline and in response to Phenylephrine and Angiotensin II. In the myocardial cells we also determined the DNA/nuclear protein interaction through electrophoretic mobility shift assay. These studies showed a significantly lower degree of ANP transcription in the presence of the mutant PEA2 site, thus demonstrating its functional significance and the biological relevance of ANP gene structural alterations.
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