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.

Metabolic syndrome (MetS) is known as a non-communicable disease (NCD) that affects more and more individuals. MetS is closely related to type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), obesity and inflammation. It is associated with T2DM due to the disturbance in insulin secretion/effect, eventually leading to insulin resistance (IR). The link between MetS and CVD is due to accelerated atherosclerosis in response to chronic inflammation. This literature review was based on a search in the PubMed database. All selected articles are written in English and cover a period of approximately 10 years (January 2014 to May 2023). The first selection used MeSH terms such as: “metabolic syndrome”, “type 2 diabetes mellitus”, “obesity”, “inflammation”, and “insulin resistance” and different associations between them. Titles and abstracts were analyzed. In the end, 44 articles were selected, 4 of which were meta-analysis studies. Currently, an individual is considered to have MetS if they present 3 of the following changes: increased waist circumference, increased triglycerides (TG), reduced high-density lipoprotein cholesterol (HDL-C), increased fasting blood glucose and hypertension. We believe this can often lead to a false diagnosis. The objective of this paper is to compile what we consider to be an appropriate panel of MetS indicators. The markers that stand out in this review are the lipid profile, anti- and pro-inflammatory function and oxidative stress. Considering the research, we believe that a complete panel, to correlate the most characteristic conditions of MetS, should include the following markers: TG/HDL-C ratio, small dense low-density lipoprotein cholesterol (SdLDL-C), lipid peroxidation markers, leptin/adiponectin ratio, plasminogen activator inhibitor-1 (PAI-1), activin-A and ferritin levels. Finally, it is important to expand research on the pathophysiology of MetS and confirm the most appropriate markers as well as discover new ones to correctly diagnose this condition.

Adventitial crosslinking is a method in current investigational stage for preventing the rupture of aortic aneurysms. It is based on the photochemical crosslinking of adventitial collagen by exposure to ultraviolet A radiation. Essentially, an adventitial top layer is generated that displays enhanced mechanical properties and imparts additional strength and stiffness to the aneurysmal wall. Looking back upon the history of aortic surgery during 1940s, the aortic film wrapping, then dubbed “cellophane wrapping”, also was a procedure employed for delaying the aneurysmal rupture. In principle, the two procedures are similar in that both result in laminar composites, although the top layers differ fundamentally from each other. This review discussed in some detail the use and clinical outcomes of the aortic wrapping with artificial films, also mentioning the contemporary procedures still grouped under this umbrella term. The focus of the review was a comparative view on two procedures, the aortic film wrapping and adventitial crosslinking. It was concluded that the methods are different in many aspects, including the mechanisms of action. In fact, the promoters of adventitial crosslinking were not aware of the prior existence of aortic film wrapping. However, the achievements of the classical wrapping, by now regarded as merely historical episodes, did not discard prior knowledge, but repurposed it in a process that led to innovative strategies.

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).

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.

The clinical manifestations of COVID-19 which mainly involve the respiratory system may however affect also cardiovascular system. There are a lot and still increasing numbers of reports revealing cardiovascular complications of COVID-19, which may occur in the acute phase as well as during longer follow-up period. The most clinically important diseases include: pulmonary embolism (PE), myocarditis, and acute coronary syndromes (ACS) as well as arrhythmias with the very common atrial fibrillation (AF) and pericarditis. In this review, cardiac imaging options in patients with and after coronavirus infection are presented, showing potential utility for expanding and improving the full and accurate diagnosis of potential complications. Echocardiography, magnetic resonance imaging, and computed tomography (CT) are considered in turn, highlighting their best advantages in patients affected by COVID.

Mitral valve prolapse (MVP) is a relatively common mitral valvulopathy and the most common cause of isolated primary mitral regurgitation (MR) requiring surgical repair. It affects about 1–3% of the general population. Although MVP is viewed as a benign condition, the association between MVP and sudden cardiac death (SCD) has been proven. Patients with MVP have a three times higher risk of SCD than the general population. The underlying mechanisms and predictors of arrhythmias, which occur in patients with MVP, are still poorly understood. However, some echocardiographic features such as mitral annulus disjunction (MAD), bileaflet MVP (biMVP), and papillary muscle (PM) fibrosis were frequently linked with increased number of arrhythmic events and are referred to as “arrhythmogenic” or “malignant”. Arrhythmogenic MVP (AMVP) has also been associated with other factors such as female sex, polymorphic premature ventricular contraction (PVC), abnormalities of T-waves, and Pickelhaube sign on tissue Doppler tracing of the lateral part of the mitral annulus. Cardiac magnetic resonance (CMR) imaging and speckle tracking echocardiography are new tools showing significant potential for detection of malignant features of AMVP. This paper presents various data coming from electrocardiography (ECG) analysis, echocardiography, and other imaging techniques as well as compilation of the recent studies on the subject of MVP.

The use of echocardiography, a straightforward and widely available technique, allows for a comprehensive assessment of the patient with hypertrophic cardiomyopathy (HCM) under both resting and stress conditions. The true prevalence of HCM has been redefined over time by this imaging approach, which has also made it feasible to pinpoint parameters that clinicians may use to stratify patients at risk for adverse cardiovascular events. The current and emerging prognostic predictors in HCM, assessed with transthoracic echocardiography at rest and during provocation, are discussed in this review.

By offering their expertise, reviewers help authors improve their work and also support editors in selecting high-quality studies, thereby reinforcing the integrity of scientific literature. Much like in a Sergio Leone film, your manuscript encounters three possible types of reviewers on its editorial journey: the Good, the Bad, and the Ugly. The Good Reviewer is, for reasons unknown, favorably disposed toward both you and your manuscript. They find it “well-written, with literary and enjoyable style”, “original and timely”, and addressing a topic that is “scientifically and socially relevant”. Their comments are respectful, constructive, and focused on minor but meaningful improvements. Unfortunately, the Good Reviewer is as rare as a white unicorn; some researchers reach the end of their careers without ever encountering one, leading them to question their very existence. The Bad Reviewer is both bad at reviewing and a bad influence on your work. They reject your manuscript, but their reasons are vague and unconvincing. Their objections are often asinine, and when you respond thoroughly and decisively, they counter with even more nonsensical arguments. They may pressure you to cite irrelevant literature—often their work or that of their colleagues. In the end, your once-solid and cohesive manuscript emerges in a far worse state than the original. None of this would have been possible without the Bad Reviewer, who, unleashed by a negligent editor, exerts their detrimental influence on your article. The Ugly Reviewer appears with unsettling regularity—at least once a month. They believe your article is truly terrible, and often, they are right. The Ugly Reviewer, though harsh, is no fool. Their critiques are brutal and unforgiving, yet accurate. Years later, you may find yourself grateful to them for preventing you from publishing work that, in hindsight, would have irreparably tarnished your already modest scientific reputation.

L-Carnitine (LC) is integral to energy production and fatty acid metabolism, facilitating the transport of long-chain fatty acids into mitochondria for β-oxidation. It modulates metabolic pathways, including pyruvate dehydrogenase activity, proteolysis, and protein synthesis, while also having anti-inflammatory and antioxidant characteristics. LC can be commonly applied to win the battle against HIV and cancer cachexia. Also, it can be recruited with the aim of improving physical and cognitive functions in athletes and the elderly. Despite these benefits, long-term LC administration has been associated to cardiovascular risks due its conversion to trimethylamine-N-oxide (TMAO) by the gut microbiota. Elevated TMAO levels are linked to atherosclerosis, oxidative stress, and an increased risk of cardiovascular disease, diabetes, and chronic kidney disease. Managing TMAO levels using dietary treatments and gut microbiota-targeting techniques, such as probiotics, may reduce these risks. This comprehensive review presents the state-of-the-art information on LC’s dual role, emphasizing the balance between its therapeutic potential and the risks of prolonged supplementation. It aims to guide clinicians and researchers in optimizing LC’s benefits while addressing its long term cardiovascular safety concerns.

Age-related atrial fibrillation (AF) is a common condition that has yet to be fully understood, with mechanisms to explain its development under investigation. Notably, cellular senescence, cardiac fibrosis, coronary ischemia, cardiac valvular disease, autonomic dysfunction, channelopathies, and immune system remodeling are processes that have been seen to occur with aging and ample evidence has shown their association with the development of AF. Despite robust therapeutic approaches, the incidence of AF continues to rise, suggesting that the dynamic, multi-faceted interactions leading to AF are incompletely understood. One of the newer mechanisms currently being investigated is the gut microbiome. Although more research is needed to understand its impact on the development of age-related AF and targets for therapies, the gut microbiome is a promising new avenue of research that may provide future benefits in AF prophylaxis or enhanced management. As the field works towards developing this knowledge, there are important questions to answer as to the optimal role of potential gut microbiome targeting therapies and their potential risks versus the benefits they provide. This commentary first summarizes the currently understood mechanisms contributing to age-related AF, which is then followed by an analysis of the current work investigating the role of the gut microbiome in the development of age-related AF, and concludes by highlighting notable questions to consider in future work on the role of the gut microbiome and its relationship to age-related AF.

Carpal tunnel syndrome (CTS) is the most common type of entrapment neuropathy and affects approximately 1% to 5% of the general population, mostly patients older than 50 years. CTS is present in various conditions and diseases and could also be an early sign of systemic transthyretin amyloidosis (ATTR), associated with amyloid cardiomyopathy and subsequent heart failure. With advances in the treatment of cardiac amyloidosis, patient prognosis could be significantly improved with an early diagnosis. Amyloidosis represents a group of disorders characterized by the extracellular deposition of destabilized protein fragments, aggregating as amyloid fibrils, thereby leading to organ dysfunction. Among these, ATTR is a significant subgroup. This study protocol aims to explore the potential association between CTS and systemic and cardiac ATTR. The study design involves a case-control approach, with assessments including physical examination, laboratory tests, electromyography, electrocardiogram, wrist ultrasound, and scintigraphy with ^99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid (^99mTc-DPD). Histopathological analysis and genetic testing will be performed when appropriate. Statistical analysis will be conducted to evaluate the relationship between CTS and ATTR. The study seeks to contribute to a better understanding of the diagnostic and therapeutic implications of identifying ATTR in patients with idiopathic CTS (ClinicalTrials.gov identifier: NCT05409833).

Exposure to ionizing radiation has recognized detrimental cancer and non-cancer health effects. These effects are now well-proven not only for high doses > 1,000 millisieverts (mSv) associated with head radiotherapy but also for moderate (100–1,000 mSv) and even low (< 100 mSv) doses, of interest for professionally exposed cardiologists. The head of interventional cardiologists is highly exposed to ionizing radiation, with possible damage to the eye and brain. Unprotected interventional cardiologists experience head radiation doses up to ten times greater than chest doses below lead aprons, with marked exposure to the left hemisphere of the brain reaching up to 2 Sv—equivalent to 10,000 chest X-rays over a professional lifetime. This narrative review aims to provide an overview of the background of radioprotection, the biological mechanisms involved, and the epidemiological evidence regarding the health effects of head exposure to ionizing radiation in invasive cardiologists. These health effects include cataracts, brain cancer, cerebrovascular diseases, neurodegeneration, and mood disorders. The evidence gathered from other exposed populations, which experienced similar eye and brain doses, has also been reviewed. This is important because the doses, risks, and effects are consistent in cases of repeated exposures, which occur more frequently for patients, and in situations involving chronic low doses, as seen with interventional cardiologists. Despite these risks, effective protective measures—such as suspended lead ceilings, curtains, and specialized eyewear—can reduce radiation exposure to near-zero levels. In some fields, like interventional cardiac electrophysiology, a groundbreaking near-zero radiation approach using non-fluoroscopic methods has been created, eliminating radiation exposure and alleviating orthopedic stress and operational discomfort. The race to zero radiation in interventional cardiology is ongoing.

Pregnancy complications such as pre-eclampsia, gestational diabetes, and intrauterine growth restriction (IUGR) not only present immediate risks to maternal and fetal health but also have long-term implications for the cardiovascular health of offspring. Emerging evidence suggests that these complications may induce epigenetic changes, which in turn predispose offspring to cardiovascular diseases (CVDs) later in life. Epigenetic modifications, including DNA methylation, histone modifications, and non-coding RNA regulation, play crucial roles in fetal development by influencing gene expression without altering the DNA sequence. Aberrant DNA methylation patterns have been observed in offspring exposed to adverse intrauterine environments, affecting genes that regulate blood pressure, lipid metabolism, and inflammation, key factors in CVDs development. Similarly, histone modifications linked to pregnancy complications can disrupt the expression of genes involved in vascular function, contributing to increased cardiovascular risk. Additionally, dysregulation of microRNAs in response to complications like gestational diabetes may influence pathways related to insulin signaling and atherosclerosis. This review synthesizes current knowledge on the epigenetic mechanisms by which pregnancy complications increase CVDs risk in offspring, highlighting potential avenues for early intervention and therapeutic strategies. Understanding these mechanisms could lead to the development of targeted interventions during pregnancy, potentially reducing the intergenerational transmission of cardiovascular risk and improving long-term health outcomes for both mothers and their children.