Micronutrients, especially vitamins, play an important role in the evolution of cardiovascular diseases (CVD). It has been speculated that additional intake of vitamins may reduce the CVD burden by acting on the inflammatory and oxidative response starting from early stages of atherosclerosis, when the vascular impairment might still be reversible or, at least, slowed down. The current review assesses the role of major vitamins on subclinical atherosclerosis process and the potential clinical implications in patients without CVD. We have comprehensively examined the literature data for the major vitamins: A, B group, C, D, and E, respectively. Most data are based on vitamin E, D and C supplementation, while vitamins A and B have been scarcely examined for the subclinical atherosclerosis action. Though the fundamental premise was optimistic, the up-to-date trials with vitamin supplementation revealed divergent results on subclinical atherosclerosis improvement, both in healthy subjects and patients with CVD, while the long-term effect seems minimal. Thus, there are no conclusive data on the prevention and progression of atherosclerosis based on vitamin supplementation. However, given their enormous potential, future trials are certainly needed for a more tailored CVD prevention focusing on early stages as subclinical atherosclerosis.

Coronary computed tomography angiography (CCTA) is a reliable screening method of patients with coronary artery disease (CAD). CCTA is capable to assess both coronary stenosis and plaque morphology, but does not provide hemodynamic characterization of the coronary lesions. However, the severity of coronary stenosis does not always reflect the hemodynamic significance of the plaque. Invasive fractional flow reserve (FFR) is considered the gold standard for the functional evaluation of a potential ischemia-causing stenosis. FFR derived from CCTA (FFR-CT) is a new noninvasive diagnostic tool, using a typically acquired CCTA, without the need for any further radiation or medication. Additional functional assessment of the coronary lesions permits a more complex characterization of CAD patients. Based on the FFR-CT examination, patients who need invasive coronary intervention can be selected more precisely, and a more personalized and optimized treatment can be provided.

Heart failure is a clinical syndrome that appears as a consequence of a structural disease, and the most common cause of left ventricular systolic dysfunction results from myocardial ischemia. Cardiac remodeling and neuroendocrine activation are the major compensatory mechanisms in heart failure. The main objective of the study is to identify the association between serum biomarkers illustrating the extent of myocardial necrosis (highly sensitive troponin as-says), left ventricular dysfunction (NT-proBNP), and systemic inflammatory response (illustrated via serum levels of hsCRP and interleukins) during the acute phase of a myocardial infarction, and the left ventricular remodeling process at 6 months following the acute event, quantified via speckle tracking echocardiography. The study will include 400 patients diagnosed with acute myocardial infarction without signs and symptoms of heart failure at the time of enrollment that will undergo a complex clinical examination and speckle tracking echocardiography. Serum samples from the peripheral blood will be collected in order to determine the inflammatory serum biomarkers. After 6 months, patients will be divided into 2 groups according to the development of ventricular remodeling, quantified by speckle tracking echocardiography: group 1 will consist of patients with a remodeling index lower than 15%, and group 2 will consist of patients with a remodeling index higher than 15%. All clinical and imaging data obtained at the baseline will be compared between these two groups in order to determine the features associated with a higher risk of deleterious ventricular remodeling and heart failure.

Kawasaki disease, also known as Kawasaki syndrome or mucocutaneous lymph node syndrome, is a pathology that causes inflammation in the walls of medium-sized arteries, with symptoms such as fever, lymphadenopathy, rash, and erythema of the eyes, lips, nose, palms, and feet. The cause is unknown, although clinical features strongly suggest an infectious etiology. We present the case of a 53-year-old woman, known with Kawasaki disease since childhood, with different associated pathologies, who presented with acute inferior ST elevation myocardial infarction.