Atherosclerosis is the leading cause of death worldwide, especially in patients with type 2 diabetes mellitus (T2D). GLP-1 receptor agonists and DPP-4 inhibitors were demonstrated to play a markedly protective role for the cardiovascular system beyond their glycemic control. Several cardiovascular outcome trials (CVOT) reported the association between using these agents and a significant reduction in cardiovascular events in patients with T2D and a high cardiovascular risk profile. Moreover, recent evidence highlights a favorable benefit/risk profile in myocardial infarction and percutaneous coronary revascularization settings. These clinical effects result from their actions on multiple molecular mechanisms involving the immune system, platelets, and endothelial and vascular smooth muscle cells. This comprehensive review specifically concentrates on these cellular and molecular processes mediating the cardiovascular effects of incretins-like molecules, aiming to improve clinicians’ knowledge and stimulate a more extensive use of these drugs in clinical practice as helpful cardiovascular preventive strategies.

Coronary artery disease (CAD) remains one of the most important causes of morbidity and mortality worldwide, and revascularization through percutaneous coronary interventions (PCI) significantly improves survival. In this setting, poor glycaemic control, regardless of diabetes, has been associated with increased incidence of peri-procedural and long-term complications and worse prognosis. Novel antidiabetic agents have represented a paradigm shift in managing patients with diabetes and cardiovascular diseases. However, limited data are reported so far in patients undergoing coronary stenting. This review intends to provide an overview of the biological mechanisms underlying hyperglycaemia-induced vascular damage and the contrasting actions of new antidiabetic drugs. We summarize existing evidence on the effects of these drugs in the setting of PCI, addressing pre-clinical and clinical studies and drug-drug interactions with antiplatelet agents, thus highlighting new opportunities for optimal long-term management of these patients.

Coronary artery disease (CAD) still represents a leading cause of mortality worldwide. Early identification of patients at the highest risk of CAD is crucial to prevent acute adverse events and reduce morbidity and mortality. The coronary artery calcium (CAC) score is a reliable cardiovascular (CV) risk index with an independent prognostic value. Guidelines recommend using it as a risk enhancer in individuals with low or moderate CV risk. However, other computed tomography (CT) measurable parameters have recently been proposed as CV risk markers. Increasing evidence demonstrates the association between epicardial fat volume and coronary atherosclerosis in chronic and acute coronary syndromes. Furthermore, other parameters obtainable from CT, such as aortic stiffness, liver fat, aortic calcium, and myocardial scarring, are under investigation. This review aims to describe all CT potential in atherosclerosis detection and cardiovascular risk assessment beyond the CAC, trying to understand how to integrate CT parameters with traditional risk factors and to improve clinicians' ability to detect CAD early, allowing appropriate therapies promptly.

Mitral annular disjunction (MAD) is a structural abnormality which is commonly seen in patients with myxomatous mitral valve disease and mitral valve prolapse. MAD is a marker of severe disease including a higher need for mitral valve intervention and more arrhythmic events, which can be a cause of sudden cardiac death (SCD). A 72-years-old man with several cardiovascular risk factors (hypertension, diabetes mellitus, obesity, previous smoking, family history of cardiovascular diseases, chronic kidney disease) experienced two pre-syncopal episodes. Therefore, he was referred to a 24-hour Holter EKG that showed a non-sustained ventricular tachycardia (VT). A transthoracic 2D echocardiogram evidenced a mitral valve prolapse with mild regurgitation, normal left and right heart dimensions and function. Elective coronary angiography was performed to rule out an ischemic aetiology of ventricular arrhythmias (multiple cardiovascular risk factors and strong familiarity for coronary artery disease). The coronary angiography revealed a stenosis of 30% of left anterior descending artery and an intermediate stenosis of right coronary artery. A myocardial perfusion scintigraphy was performed to evaluate the intermediate coronary stenosis. The scintigraphy showed numerous focal perfusion abnormalities non indicative for coronary disease but rather for a degenerative or inflammatory disease. Indeed, we decided to perform a cardiac magnetic resonance (CMR). The CMR revealed a MAD with detachment of the root of the mitral annulus from the postero-lateral ventricular myocardium during systole, without areas of myocardial fibrosis evidenced by late gadolinium enhancement (LGE). Factors for high risk of SCD, such as fibrosis affecting the infero-basal left ventricle free wall or the papillary muscles, family history of SCD, personal history of complex ventricular arrhythmias, were not represented in our case. Therefore, we opted for a medical therapy with beta-blockers and a careful follow-up. MAD is an under-recognized cause of ventricular arrhythmias and SCD, generally associated to mitral valve prolapse. Echocardiography and CMR can identify and quantify MAD. A comprehensive evaluation, including multimodality imaging and clinical history, is mandatory for risk stratification of SCD and for optimal treatment.

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