Cardiovascular disease is most frequently caused by the development and progression of atherosclerosis. When coronary arteries are afflicted, and the stenoses caused by atherosclerotic plaques are severe enough, the metabolic supply-and-offer balance is disturbed, leading to myocardial ischemia. If atherosclerotic plaques become unstable and local thrombosis develops, a myocardial infarction occurs. Sometimes, myocardial ischemia and infarction may result in significant and irreversible heart failure. To prevent severe complications, such as acute coronary syndromes and ischemia-related heart failure, extensive efforts have been made for developing biomarkers that would help identify patients at increased risk for cardiovascular events. In this two-part study, we attempted to provide a review of existing knowledge of blood biomarkers that may be used in this setting. The first part of this work was dedicated to conventional biomarkers, which are already used in clinical practice. In the second part, here presented, we discuss emerging biomarkers which have not yet become mainstream.

Atherosclerosis is the main cause of cardiovascular disease worldwide. The progression of coronary atherosclerosis leads to coronary artery disease, with impaired blood flow to the myocardium and subsequent development of myocardial ischemia. Acute coronary syndromes and post-myocardial infarction heart failure are two of the most common complications of coronary artery disease and are associated with worse outcomes. In order to improve the management of patients with coronary artery disease and avoid major cardiovascular events, several risk assessment tools have been developed. Blood and imaging biomarkers, as well as clinical risk scores, are now available and validated for clinical practice, but research continues. The purpose of the current paper is to provide a review of recent findings regarding the use of humoral biomarkers for risk assessment in patients with heart disease.

We report the case of a 69-year-old female patient in which echocardiography and cardiac magnetic resonance imaging were used to diagnose a patient presenting with heart failure with preserved ejection fraction (HFpEF) due to Loeffler endocarditis. Loeffler endocarditis is an uncommon cause of heart failure with preserved ejection fraction, triggered by eosinophil and lymphocyte infiltration of the endomyocardium, followed by the formation of thrombus in the afflicted area, and eventually fibrosis. This condition is due to an increased number of eosinophils associated with allergies, infections, systemic conditions, as well as malignancies and hypereosinophilic syndrome. Loeffler endocarditis can lead to serious complications, such as progressive heart failure, systemic thromboembolic events, or arrhythmias (including sudden cardiac death).

Objectives: The presence of a bicuspid aortic valve (BAV) is known to alter transvalvular flow and increase shear stress on the ascending aorta, contributing to alterations in aortic geometry and the progression of BAV-related aortopathy. The purpose of the current study was to characterize aortic flow abnormalities and their associations with aortic geometry and ventricular mechanics using cardiac magnetic resonance imaging (CMR). Methods: In this prospective cross-sectional study, 56 young adults with CMR-confirmed BAV and 56 age- and sex-matched healthy volunteers underwent standardized CMR. Biventricular volumes and function, LV global longitudinal strain (LV-GLS), LV torsional mechanics, ascending aortic geometry, pulse-wave velocity, aortic distensibility, and two-dimensional phase-contrast-derived forward and backward flow parameters were quantified. Associations between myocardial mechanics and haemodynamic variables were assessed using correlation analyses and multivariable linear regression. Results: Compared with healthy controls, patients with BAV exhibited preserved LV ejection fraction but impaired LV-GLS, reduced LV torsion, increased aortic stiffness, and a significantly greater backward-flow burden despite similar net aortic flow (all p < 0.001). Higher peak backward-to-forward flow-rate ratios were associated with less negative LV-GLS (p = 0.006), whereas greater aortic regurgitant volume was also associated with impaired longitudinal deformation (p = 0.001). In multivariable analysis, LV-GLS and aortic regurgitant volume remained associated with the peak backward-to-forward flow-rate ratio within the specified model, whereas ascending-aortic dimensions were not. The final model explained 52% of the variability in backward-flow burden. Conclusions: CMR identified a subclinical ventricular-aortic phenotype in young adults with BAV characterized by altered LV mechanics, increased aortic stiffness, and greater relative backward-flow burden despite preserved conventional LV systolic function. The association between backward-flow burden and LV longitudinal mechanics suggests that these abnormalities may represent interrelated manifestations of BAV disease; however, their temporal and causal relationships cannot be established from this cross-sectional study.