Drawing insights from a spectrum of in vitro, in vivo experimental, and clinical studies, this review illuminates the underlying mechanism by which iodinated contrast media (ICM) exerts an indirect genotoxic effect. The mechanism involves the photoelectric effect induced by iodine molecules, thereby augmenting radiation attenuation and subsequently elevating the locally absorbed radiation dose. The ensuing generation of secondary electrons from each photoelectric absorption interaction triggers molecular reactions, culminating in discernible DNA damage, notably in the form of DNA double-strand breaks. A convergence of evidence from in vitro, experimental, and clinical investigations underscores a consistent pattern: the addition of iodine contrast linearly heightens the absorbed radiation dose and associated DNA damage. This quantification was evident through alterations in attenuation and the manifestation of double-strand breaks in circulating lymphocytes, serving as an intermediate endpoint and a potential long-term indicator of cancer. The observed surplus of DNA damage in contrast-enhanced images compared to non-contrast images ranged notably from +30% to +200%. This broad range accentuates a substantial amplification effect on radiation-induced damage, particularly noteworthy at clinically relevant iodine doses. Crucially, this effect remains unaffected by brands or manufacturers and exhibits a robust, exclusive correlation with the concentration of iodine in the bloodstream. The significant augmentation of absorbed dose and genotoxic impact of X-rays due to the use of contrast agents warrants critical attention within the medical community. This often-unacknowledged genotoxic influence may play a pivotal role in elevating cancer risks among patients undergoing radiation-based procedures, necessitating a reconsideration of risk assessment protocols and clinical practices.

Myocardial bridging is a congenital defect characterized by the course of a segment of the coronary arteries within the heart muscle most frequently affecting the left anterior descending coronary artery (LAD). Patients with myocardial bridging may present with episodes of exertional anginal chest pain. The gold standard for non-invasive diagnosis of myocardial bridge is coronary computed tomography angiography (CCTA), which allows anatomical characterization. Coronary flow velocity reserve (CFVR) of the LAD on stress echocardiography (SE) can play an important role in the diagnosis of myocardial bridging of the LAD; a relationship between CVFR-LAD and coronary inflammation by estimating the attenuation of peri-coronary adipose tissue at CCTA has been demonstrated in patients without obstructive ischaemic heart disease. Therefore, coronary inflammation localized to the LAD has been assessed in patients diagnosed with myocardial bridging of the LAD and previous SE with CFVR-LAD in a case series.

Coronary vasospasm stands as a widely acknowledged and frequent culprit behind chest pain, acute coronary syndrome, and sudden cardiac death, yet it remains a challenging diagnosis. Current guidelines recommend invasive coronary function testing to assess pathophysiology and mechanisms and to define treatment. In reality, this protocol is rarely applied, because it necessitates extended occupation of the cath lab, repetitive administration of nephrotoxic iodine contrast agents, the need for repeated testing on both coronary arteries leading to considerable radiation exposure, and significant direct expenses. The promising perspective for vasospasm testing is a noninvasive approach with advanced echocardiographic techniques, such as transthoracic Doppler echocardiography, with more sensitive indicators of ischemia. Hyperventilation and exercise tests are used for vasospasm directed testing, with assessment of the new parameters: coronary flow velocities and reserve, allowing to see deeper into macro and microvascular pathophysiology. Association between coronary flow, global longitudinal strain and microvascular dysfunction (MVD) and impaired values at hyperemia was previously demonstrated. Reduction in coronary flow velocity (CFV) despite heightened myocardial oxygen consumption and double product during hyperventilation are indicative of coronary vasospasm. Normal coronary angiography finding in patients with documented evidence of ischemia should initiate additional diagnostic testing in order to increase the yield of specific diagnosis in patients with suspected vasospasm, which could help to personalize treatment and prognosis. In order to achieve this, non-invasive provocative stress echocardiography tests should be included in the diagnostic workup. This approach, characterized by its simplicity, feasibility, safety, and efficacy, is currently undergoing extensive testing on a large scale.

Lipoprotein(a) [Lp(a)] is composed of a low-density lipoprotein (LDL) and glycoprotein (a)—apolipoprotein(a) [apo(a)]. The size and concentration of Lp(a) in serum can vary among individuals and is determined by genetic factors. The environmental factors, diet, and physical activity have a negligible effect on Lp(a) level. Observational, epidemiological, and genetic studies improved that high levels of Lp(a) > 50 mg/dL (> 125 nmol/L) have been associated with an increased risk of myocardial infarction (MI), stroke, and calcific aortic valve stenosis (CAVS). It is recommended to measure Lp(a) at least once in adults to identify individuals with a high cardiovascular risk. This screening is particularly important in certain populations, including: youth with a history of ischemic stroke or a family history of premature atherosclerotic cardiovascular disease (CVD; ASCVD) or high Lp(a), individuals with recurrent cardiovascular events despite optimal hypolipemic treatment and no other identifiable risk factors or patients with familial hypercholesterolemia (FH). Considering Lp(a) levels in the evaluation of cardiovascular risk can provide valuable information for risk stratification and management decisions. However, it’s important to note that the treatments of elevated level of Lp(a) are limited. In recent years, there has been ongoing research and development of new drugs targeting Lp(a): pelacarsen—antisense oligonucleotide (ASO), and olpasiran—a small interfering RNA (siRNA).

Atherosclerosis is a chronic disease, characterized by chronic inflammation, endothelial dysfunction, and lipid deposition in the vessel. Although many major, well-identified risk factors for atherosclerosis [e.g., hyperlipidemia, hypertension, type 2 diabetes (T2D), smoking habit, and obesity] explain a lot about the risk, there is a considerable number of patients who develop atherosclerotic damage and undergo adverse events without presenting any of these established modifiable risk factors. This observation has stimulated an urgent need to expand knowledge towards the identification of additional, less established risk factors that may help in the assessment of risk and fill the gap of knowledge in the cardiovascular (CV) setting. Among them, the hypothesis of a possible relationship between viral infectious agents and atherosclerosis has risen since the early 1900s. However, there is still a great deal of debate regarding the onset and progression of CV disease in relation to the roles of the pathogens (as active inducers or bystanders), host genomic counterparts, and environmental triggers, affecting both virus abundance and the composition of viral communities. Accordingly, the aim of this review is to discuss the current state of knowledge on infectious agents in the atherosclerotic process, with particular focus on two environmental-related viruses, as examples of familiar (influenza) and unfamiliar [severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)] disease triggers.