Editorial [ Hot Topic: Modifying Cardiovascular Risk Factors: Novel Cardiovascular Targets for Treatment by Noninvasive Imaging Techniques (Executive Editors: Aurelio Leone and Luigi Landini) ]

Cardiovascular risk factors, whatever they may be approached to be studied - and there are a lot of approaches: clinical, biological, metabolic, epidemiologic, statistic and diagnostic - lead all to a proven result that is increasing the incidence of cardiovascular pathology. The early and careful assessment of cardiovascular risk factors as well as their influence on functional and metabolic steps of the heart permit to establish those preventive measures that may fight myocardial damage. Cardiovascular risk factors often determine myocardial dysfunction either structurally or functionally and assessing its degree and type may be particularly useful. Diagnostic evidence of physiopathologic features of myocardium and role of the major cardiovascular risk factors may be, nowadays, carried out by the use of non-invasive imaging techniques that, time by time, have met significant progresses in methodology and applying. Resting myocardial blood flow, myocardial metabolism, and cardiovascular function may be correctly interpreted by different imaging techniques with results that depend on type of applied methodology, since there are procedures that focus on some cardiovascular patterns and some on others. The paper of Landini et al. [1] introduces the prominent in vivo cardiovascular imaging modalities such as magnetic resonance imaging, nuclear imaging and ultrasound from both the physical and molecular imaging perspectives. A brief introduction to the molecular imaging principles is also reported. Special emphasis has been given to the imaging parameters of sensitivity and spatial resolution, and the trade-off between spatial resolution, image contrast and target size. Passacquale et al. [2] underline the typical morphology of atherosclerotic plaque as well as the role of imaging techniques to assess it. Detection of early atherogenesis and characterization of plaque feature are the major end-points of research in cardiovascular imaging. Different techniques have been proposed as an instrument for morphological and functional study of vascular walls. Clinical evidence suggests the usefulness of atherosclerosis imaging to better define the cardiovascular risk stratification, the prognosis and the therapeutic approach to patients. A very interesting study was conducted by Virdis et al. [3] on the role, diagnosis and relationship between hypertension and endothelial dysfunction. A large body of evidence indicates that patients with essential hypertension, and even more those with complicated hypertension, display endothelial dysfunction characterized by impaired NO availability secondary to oxidative stress production. A dysfunctioning endothelium is an early marker of the development of atherosclerotic changes and can also contribute to cardiovascular events. Vascular reactivity tests represent the most widely used methods in the clinical assessment of endothelial function. In the last two decades, many studies have evaluated the endothelium in hypertensive patients, using different techniques. Several methodologies were developed to study microcirculation (resistance arteries and arterioles) and macrocirculation (conduit arteries), both in coronary and peripheral vascular districts. No available test to assess endothelial function has sufficient sensitivity and specificity to be used in clinical practice. Therefore, the optimal methodology for investigating the multifaceted aspects of endothelial dysfunction is still under debate. Only the growing concordant results from different reproducible and reliable methods exploring endothelial function with different stimuli will support and strength experimental findings, thus providing conclusive answers in this area of research. Leone et al. [4] debate about the main morphological patterns that characterize myocells as an effect of smoking exposure. Two morphologic features may be seen as a main result of the cardiovascular cell damage caused by cigarette smoking: myocardial cell necrosis and smoke cardiomyopathy that, however, can lead to cell necrosis in case of chronic prolonged exposure to tobacco smoke. Both these pathologic patterns recognize hypoxia as basic mechanism. Cardiovascular cell damage may involve either myocardial cell or coronary artery wall determining a varied but wide spectrum of alterations. Necrosis may be well defined as a result of those morphologic changes which follow cell death in a living tissue or organ with partial or total loss in their function. All infarcts of the heart muscle belong to the group of necrotic lesions, but not all cardiac necroses are necessarily infarcts. Coronarogenic or non-coronarogenic mechanism following a direct action of tobacco compounds on myocardial cells may induce myocardial cell necrosis. Smoke cardiomyopathy is probably the most typical evidence of cellular damage induced by cigarette smoking on the myocardium.