Tuberculosis (TB) continues to pose a significant public health burden in endemic regions, remaining a leading cause of morbidity and mortality. Although TB is associated with a range of complications, the occurrence of intracardiac thrombus is an exceptionally rare manifestation. We report the case of a 62-year-old male with active pulmonary TB, who had been on anti-tubercular therapy for one month and presented with recurrent syncope and exertional dyspnea. Transthoracic 2D echocardiography revealed a large, mobile thrombus in the left ventricular apex. Evaluation for underlying hypercoagulable states was unremarkable. The patient was managed with anticoagulation therapy in conjunction with ongoing anti-tubercular treatment. This case underscores the importance of clinical vigilance for rare thrombotic complications in TB to facilitate timely diagnosis and appropriate management.

Preterm birth, defined as delivery before 37 weeks of gestation, represents a global health concern linked to substantial cardiovascular risk later in life. Individuals born preterm, especially at earlier gestational ages, exhibit increased rates of hypertension, heart failure, and ischemic heart disease. The underlying mechanisms include disrupted fetal programming, impaired vascular remodeling, chronic neonatal inflammation, neuroendocrine immaturity, and epigenetic alterations. This review synthesizes current epidemiological evidence from large cohort studies and meta-analyses, integrating mechanistic insights from developmental biology. We discuss distinct prematurity categories—extremely preterm (< 28 weeks), very preterm (28–32 weeks), and moderate to late preterm (33–37 weeks)—highlighting their association with graded cardiovascular risk. Recent findings emphasize the role of non-transmitted parental genes and prenatal environmental toxic metal exposure as additional critical factors influencing fetal cardiovascular programming. A total of 57 articles, identified through a systematic search of PubMed, Embase, and Cochrane databases, were included to address these topics comprehensively. Early identification of preterm-born individuals as a high-risk cardiovascular group is essential for targeted screening, prevention, and interventions from childhood into adulthood. Future studies leveraging multi-omics and epigenetic approaches will further clarify these mechanisms, informing evidence-based guidelines to reduce cardiovascular morbidity associated with preterm birth.

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.

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.

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.

The oxidation of lipoproteins has a key role in the development of atherosclerosis, a condition where plaque builds up in artery walls. Research shows that when low-density lipoprotein (LDL) oxidizes, it speeds up atherosclerosis. Oxidized LDL (Ox-LDL) causes many pathologic scenarios that lead to atherosclerosis. It was suggested as a fundamental player in endothelial dysfunction, creating foam cells, and triggering inflammation in artery walls. How Ox-LDL contributes and interacts with specific receptors on endothelial cells is crucial to these effects. This article aims to shed light on LDL oxidation, the stages of the process, and how Ox-LDL promotes atherosclerosis. A comprehensive search was conducted across various databases, including PubMed, Google Scholar, Scopus, and Ovid, to identify literature and studies that discuss Ox-LDL and their involvement in the pathogenesis of atherosclerosis and cardiovascular diseases, thereby establishing a well-defined perspective on the subject. This review will provide a closer look at the Ox-LDL particle, the different forms and stages of oxidation, and the role of various LDL receptors involved in LDL uptake and breakdown focusing on how they contribute to atherosclerosis. Then, it will discuss the role of scavenger receptors and their contribution to the uptake of Ox-LDL and how this contributes to the development of atherosclerosis.

We present the case of a woman admitted for an acute ST-segment elevation myocardial infarction. Emergency catheterization was conducted, revealing diffuse lesions affecting 70% of the anterior descending artery from the mid to the distal third but with ventriculography compatible with Takotsubo syndrome. Two magnetic resonances were performed 90 days apart, confirming the unusual coexistence of Takotsubo syndrome and transmural infarction in the same event.

Data on the use of mechanical circulatory support devices in pregnant women are limited. A 27-year-old woman at 27 weeks and 6 days of gestation was supported by three different mechanical circulatory support devices due to cardiogenic shock. She came into spontaneous labor, which was complicated by major hemorrhage at the cannulation site, fetal distress, and transverse position, requiring emergency cesarean section. The postpartum period was complicated by intra-abdominal bleeding and arterial occlusion of lower extremity. When using mechanical circulatory support devices in pregnant women, a multidisciplinary approach is recommended.

Cardiovascular diseases, particularly ischemic heart disease (IHD), are the leading cause of mortality globally, accounting for 16% of deaths. Effective management of ischemic cardiomyopathy (ICM) is crucial, as outlined in the latest European Society of Cardiology (ESC) guidelines for chronic coronary syndrome (CCS). The guidelines emphasize a structured approach comprising four key steps: a general clinical evaluation to exclude non-cardiac causes, cardiac examination, and likelihood estimation using echocardiography, diagnostic testing such as stress echocardiography and coronary CT angiography, and treatment involving lifestyle changes and medication, alongside potential revascularization. The review underscores the importance of coronary angiography and functional assessments in diagnosing ischemic heart failure (IHF) and guiding treatment strategies. Non-invasive imaging techniques, including stress echocardiography and myocardial perfusion scintigraphy, are valuable for assessing ischemia and myocardial viability while reducing unnecessary invasive procedures. Coronary CT angiography is also examined for its procedural advantages and risks. A comparative analysis of diagnostic modalities highlights the strengths and limitations of each technique, emphasizing the need for individualized approaches based on patient characteristics. The ESC 2024 guidelines advocate for a patient-centered imaging strategy based on the likelihood of coronary artery disease (CAD) while addressing the economic and environmental impacts of imaging practices. Overall, implementing these guidelines and leveraging diverse imaging modalities can optimize management strategies for IHD, ultimately improving patient outcomes.

Papillary muscle rupture is a rare but fatal complication of acute myocardial infarction. The incidence of this complication has been reduced to less than 0.1% of patients due to the advent of primary percutaneous coronary intervention. Cardiogenic shock and acute pulmonary edema are the most common clinical presentations. In this review, we describe the role of transthoracic and transesophageal echocardiography in identifying the type, location, and hemodynamic consequences of the three different echocardiographic patterns of papillary muscle rupture. This information is crucial for managing medical therapy and determining the appropriate surgical or percutaneous treatment.

Pulmonary congestion is a key determinant of heart failure, but for a long time it has been an elusive target for the clinical cardiologist in the pre-B-line era, despite research efforts of Carlo Giuntini, a pneumologist who attempted the quantification of lung water in the seventies with too insensitive chest X-ray lung water score, too cumbersome nuclear medicine, and too complex invasive thermodilution techniques. Daniel Lichtenstein, is a French intensivist who first discovered lung ultrasound as a sign of extravascular lung water in 1997. B-lines (also known as ultrasound lung comets) detectable by lung ultrasound arise from the pleural line, extend towards the edge of the screen, and move synchronously with respiration. In cardiology, B-lines were introduced in 2004 and are now the dominant technique for research applications and clinical purposes. B-lines showed a prognostic value in several clinical scenarios, largely independent and additive over echocardiographic predictors such as ejection fraction. The methodology became user-friendly in the last years, with a reduction of the scanning sites from the original 28 to a simplified 4-site scan now extracting information on lung water in < 1 minute. More recently, B-lines were also studied during physical and pharmacological stress. Signs of pulmonary congestion are found during stress in 1 out of 3 all-comers with normal findings at rest. Artificial intelligence applied to ultrasound and clinical data allows for the detection of B lines, their quantification, and the assessment of their nature. The B-lines phenotype can cluster around different endotypes: dry (in systemic sclerosis and lung interstitial fibrosis); wet (water); sterile (as in cardiogenic edema); infective (as in COVID-19 and interstitial pneumonia); right heart-sided (as in pulmonary arterial hypertension); left-heart sided (as in heart failure or valvular heart disease). Artificial intelligence B-lines and pocket-size insonation of the B-lines-driven decongestion therapy are now on the horizon.

Ischemic heart disease (IHD) is a major global health issue, frequently resulting in myocardial infarction and ischemic cardiomyopathy. Prompt and precise diagnosis is essential to avert complications such as heart failure and sudden cardiac death. Although invasive coronary angiography remains the gold standard for high-risk patients, noninvasive multimodality imaging is becoming more prevalent for those at low-to-intermediate risk. This review evaluated the current state of multimodality imaging in IHD, including echocardiography, nuclear cardiology, cardiac magnetic resonance imaging (MRI), computed tomography (CT) angiography, and invasive coronary angiography. Each modality has distinct strengths and limitations, and their complementary use provides a comprehensive assessment of cardiac health. Integrating artificial intelligence (AI) into imaging workflows holds promise for enhancing diagnostic accuracy and efficiency. AI algorithms can optimize image acquisition, processing, and interpretation of complex imaging data. Emerging technologies like 4D flow MRI, molecular imaging, and hybrid systems [e.g., positron emission tomography (PET)/MRI, PET/CT] integrate anatomical, functional, and molecular data, providing comprehensive insights into cardiac pathology and potentially revolutionizing the management of IHD. This review also explored the clinical applications and impact of multimodality imaging on patient outcomes, emphasizing its role in improving diagnostic precision and guiding therapeutic decisions. Future directions include AI-driven decision support systems and personalized medicine approaches. Addressing regulatory and ethical challenges, such as data privacy and algorithm transparency, is crucial for the broader adoption of these advanced technologies. This review highlighted the transformative potential of AI-enhanced multimodality imaging in improving the diagnosis and management of IHD.

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.

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.

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).

Chagas disease is a systemic illness characterized by acute and chronic phases. If untreated, it can lead to dysfunction of vital organs, notably the heart, ultimately resulting in heart failure. Transmission primarily occurs through the feces of triatomine insects carrying the protozoan parasite Trypanosoma cruzi, either via a bite wound or intact mucous membranes. Diagnosis of Chagas disease involves serological tests, electrocardiographic findings, and imaging studies. A 58-year-old male patient from Peru with chronic dilated cardiomyopathy underwent evaluation at a tertiary care hospital. Given the uncertain etiology, a comprehensive diagnostic approach was adopted, emphasizing the pivotal role of cardiovascular magnetic resonance imaging and computed tomography angiography in managing chronic cardiomyopathy of Chagas disease. Leveraging these imaging modalities together could augment our ability to evaluate myocardial inflammation and tailor therapeutic strategies accordingly.

Redo surgical aortic valve replacement (SAVR) has long been the standard treatment for severe symptomatic aortic stenosis (AS) and insufficiency, but transcatheter aortic valve replacement (TAVR) has emerged as a less invasive alternative, particularly for symptomatic AS. With calcification being a primary mechanism behind structural valve degeneration, factors such as patient characteristics and the type of bioprosthetic valve play crucial roles in determining risk. Valve-in-valve TAVR (ViV TAVR) has gained prominence as a viable alternative to redo SAVR in recent years. Echocardiography plays a pivotal role in patient selection, procedural guidance, and post-procedural evaluation in ViV TAVR. From pre-procedural assessment using transthoracic and transesophageal echocardiography to intra-procedural guidance and post-procedural follow-up, echocardiography aids in ensuring procedural success and monitoring valve function. Decision-making between redo SAVR and ViV TAVR involves multidisciplinary teams considering various factors like patient risk profile, anatomical considerations, and technical feasibility. While redo SAVR remains preferred for younger patients with lower risk, ViV TAVR is increasingly considered for older patients or those with higher reoperation risks. Factors such as coronary artery obstruction risk, patient-prosthesis mismatch, and paravalvular leak guide treatment decisions. Procedural techniques in ViV TAVR have evolved to minimize complications and optimize outcomes. Factors like access route selection, valve choice, and procedural guidance techniques significantly impact procedural success. Balloon valve fracture and preventive strategies against coronary obstruction are crucial considerations during the procedure. Post-procedural evaluation involves assessing clinical and hemodynamic outcomes, with long-term studies indicating favorable results but highlighting the importance of careful evaluation of transprosthetic gradients and valve function. ViV TAVR offers promising outcomes but requires meticulous patient selection, procedural planning, and post-procedural management to ensure optimal results.

Pneumopericardium, the presence of air within the pericardial sac, is a rare but critical condition that can lead to severe complications such as tension pneumopericardium and cardiac tamponade, causing hemodynamic instability and necessitating immediate intervention. Various etiologies include congenital defects, post-surgical complications, infections, and trauma. Malignancies, such as advanced esophageal cancer or lung carcinoma, can also cause pneumopericardium via fistula formation. Multimodal imaging, including chest X-ray, echocardiography, and computed tomography (CT), is essential for diagnosis. This case report discusses a 65-year-old male with advanced pancreatic adenocarcinoma who developed pneumopericardium following the removal of a left lobe liver drainage catheter. Initial CT imaging revealed liver lesions suspicious for metastatic disease or abscess, leading to drainage procedures. Following the removal of the drainage tube, the patient experienced respiratory distress and hypotension, and computed tomography pulmonary angiogram (CTPA) revealed pneumopericardium, likely due to a fistula formed between the abscess and pericardium. Despite no echocardiographic signs of tamponade, the patient’s persistent hypotension warranted CT-guided pericardiocentesis, resulting in gradual blood pressure improvement. This case highlights the intricate interplay between malignancy, infection, and procedural complications in developing pneumopericardium. It emphasizes the need for a multidisciplinary approach and the importance of considering both the quantity and rate of air accumulation when assessing the risk of hemodynamic compromise. The patient’s hemodynamic instability and subsequent improvement following pericardiocentesis underscore the critical role of timely intervention in managing this condition.

Vascular aging is recognized as one of the hallmarks of atherosclerosis. Currently, a growing body of evidence suggests that there exists a mutual crosstalk between telomere dysfunction and mitochondrial dysmetabolism during the process of vascular senescence. This underscores the importance of comprehensively studying the molecular mediators involved in this complex and intricate connection. In pursuit of this goal, the “VICTORIA” protocol entails a prospective single-center cohort study aimed at recruiting patients undergoing coronary angiography at Niguarda Hospital in Italy. The primary objective is to explore potential associations between peripheral markers of cell aging (telomere length and mtDNA content), dysregulation of non-coding RNA [specifically lncRNA TERRA and mitochondrial microRNA (MitomiR)], and the varied presentations of ischemic heart disease (stable angina, unstable angina, NSTEMI, and STEMI). Furthermore, we aim to investigate whether these markers correlate with vulnerable plaque characteristics, as assessed by optical coherence tomography findings. Additionally, systemic levels of pro-inflammatory biomarkers and novel indicators of senescence will be assessed. Patients will be followed up at 1 year to monitor primary outcomes including mortality, myocardial infarction, stroke, unplanned revascularization, and rehospitalization. The anticipated findings of this study hold promise for advancing our understanding of the telomere-mitochondria crosstalk, potentially paving the way for novel treatment modalities and refined risk stratification approaches for acute coronary syndrome.

Pulmonary embolism (PE) is the third leading cause of cardiovascular mortality worldwide. Percutaneous mechanical thrombectomy is indicated in patients with contraindications to thrombolysis. Complications include atrial or ventricular perforation causing tamponade. We describe one case of pericardial tamponade in an elderly woman who underwent thrombectomy for acute PE. An 88-year-old woman presented with acute shortness of breath. She was tachycardic, oxygen saturation of 80% and blood pressure of 95/57 mmHg. Bedside ultrasound showed a dilated right ventricle. Electrocardiogram showed large S wave in lead I, Q wave and inverted T wave in lead III. Computed tomography (CT) angiogram of the chest revealed an extensive saddle PE. Tissue plasminogen activator was deferred given patient’s age. Full dose anticoagulation was started and she underwent a successful percutaneous thrombectomy with FlowTriever device. Two hours later, she developed severe back pain and hypotension to 88/63 mmHg. Hemoglobin dropped from 13.7 g/dL to 8.8 g/dL. CT chest angiogram showed dense pericardial effusion, likely hemopericardium, with mass effect on the heart. Bedside pericardiocentesis was attempted and converted to pericardial window given sustained hypotension. She went into cardiac arrest. Emergent thoracotomy revealed significant hemothorax. The pericardium was opened yielding a blue, globally ischemic, and non-contracting heart. Cardiac massage and intra-cardiac epinephrine attempted unsuccessfully. Percutaneous thrombectomy using the large bore design FlowTriever system has shown promising results in reducing clot burden and improving hemodynamics. Attention must be paid to life threatening complications such as cardiac tamponade which can be precipitated by using these devices.

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.

Left ventricular (LV) function is typically evaluated through LV ejection fraction (EF), a robust indicator of risk, showing a nonlinear increase in mortality rates below 40%. Conversely, excessively high EF values (> 65%) also correlate with elevated mortality, following a U-shaped curve, with its nadir observed between 50% and 65%. This underscores the necessity for improved identification of the hypercontractile phenotype. However, EF is not synonymous with LV contraction function, as it can fluctuate independently of contractility due to variations in afterload, preload, heart rate, and ventricular-arterial coupling. Assessing the contractile status of the LV requires more specific metrics, such as LV elastance (or contractile force) and global longitudinal strain. Current guidelines outline various parameters for a more precise characterization of LV contractility, yet further research is warranted for validation. The true hypercontractile phenotype is evident in cardiac pathologies such as hypertrophic cardiomyopathy, ischemia with angiographically normal coronary arteries, Tako-tsubo syndrome, heart failure with preserved EF, and may also stem from systemic disorders including anemia, hyperthyroidism, liver, kidney, or pulmonary diseases. The hypercontractile phenotype constitutes a distinctive hemodynamic substrate underlying clinical manifestations such as angina, dyspnea, or arrhythmias, presenting a target for intervention through beta-blockers or specific cardiac myosin inhibitors. While EF remains pivotal for clinical classification, risk stratification, and therapeutic decision-making, integrating it with other indices of LV function can enhance the characterization of the hypercontractile phenotype.

While authorship practices can vary across different disciplines, authorship should reflect the individuals who have made a substantial contribution to the research project, take public responsibility for the paper’s content, and agree to its submission for publication. In real life, the article is usually authored by at least one truly genuine author and some parasitic authors. The first author and the last author are especially important. The middle authors are less important, and their participation is often wrongly seen as an inconsequential decorative favor. The honorary author, a gift or guest author, is added as a bonus to please someone higher in the hierarchy than the submitting author. This practice is believed to enhance the chances of publication, but usually, the excess of honorary authors will make reviewers more critical. A ghost author contributed substantially but it does not appear in the list of authors to avoid declaring an overt conflict of interest. The gold author is someone paid by a third party in direct or indirect forms, and capable of writing and signing everything asked by the payer, including overstating the merits of a new drug or ignoring its drawbacks. A fake author does not exist, and while it may seem humorous it is a breach of scientific integrity and can lead to serious consequences for the individuals involved. With Chat-generative pre-trained transformer (Chat-GPT), artificial intelligence may contribute decisively to the article content and presentation. Overall, it is important to maintain high standards of integrity and transparency in authorship practices to ensure that research findings are trustworthy and reliable. The reputation of your work is in the hands of your coauthors, so choose them carefully and make sure they share your commitment to scientific integrity.

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.

Congenital heart defects (CHD) represent the most frequent congenital anomalies among newborns, as well as the leading cause of spontaneous abortion, stillbirth, neonatal and infant death. CHD have been recognized as multifactorial diseases, with environmental contaminants as potential contributors to the etiopathogenesis of CHD. Toxic elements, such as arsenic (As), cadmium (Cd), lead (Pb), and mercury (Hg) are known to be associated with adverse reproductive outcomes and certain congenital anomalies, however their association with the risk for CHD remains inconsistent. This review summarizes the updated evidence on the CHD-associated risk related to exposure to As, Cd, Hg, Pb during pregnancy, reporting the main findings from epidemiological and experimental studies and the underlying molecular mechanisms. Additionally, being diet the major source of these elements in the general population, after having identified the main vectors of toxic metals in food, possible remediation strategies to reduce diet-related risks are also described. Among these, a novel, consumer-centered approach in developing new foods is discussed, considering not only the nutritional characteristics of edible compounds foods are made up of, but also their organoleptic features, making the food even more appealing to the consumer. Overall, current data support the association of maternal exposure to As and Pb with increased risk for CHD, although significant associations have only been observed for total and/or specific subgroups. On the other hand, the evidence of association for Cd and Hg exposure in pregnancy with CHD in the offspring remains, yet, quite speculative. Further large prospective cohort studies and insights into the molecular and biomolecular processes of these relationships are warranted to further explore and/or verify these findings.

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.

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.

Alcohol drinks, especially wine, have been described since 6,000 B.C. For many years in modern medicine, wine in moderation has been considered healthy for cardiovascular prevention, i.e., recommended by nutrition committees. Some regional guidelines still recommend one to two standard drinks per day. By the very recent (January 2023), World Health Organization and Canadian Guidance on alcohol emphasize that any alcoholic drink is hazardous to the health and the safe amount is zero. The risk starts with every single drop. It was also nicely summarized in the manuscript “Alcohol-dose question and the weakest link in a chemical interplay” (Explor Cardiol. 2023;1:15–25. doi: 10.37349/ec.2023.00003) especially from the standpoint of a researcher in the cardiovascular arena. The newest recommendations are based on observational studies and their meta-analysis, therefore establishing associations, pointing out that alcohol may somewhat prevent cardiovascular diseases and diabetes type 2, but with a significant increase in non-cardiovascular morbidity and mortality, especially cancers. Previous recommendations, therefore, may be obsolete as they were based on studies where abstainers from alcoholic beverages had inherent higher risks. The current controversy with conflicting guidelines for alcoholic beverage consumption in the era of precision medicine may stimulate more fundamental investigations up to genetic ones and find the cause-effect relations. In the era of precision medicine, it may come closer to discovering the causes of cancers and many other diseases, enabling predictions of reactions to alcoholic beverages by each person, not just in the population.

The deleterious consequences of alcohol consumption are extensively documented across various dimensions of human health, encompassing somatic disorders such as nervous system impairments, digestive system abnormalities, and circulatory dysfunctions, in addition to socio-psychological aspects. Within the domain of cardiology, a substantial portion of the ongoing scientific discourse centers on elucidating the toxic dose of alcohol. Presented herewith are the findings from a comprehensive review of the latest publications pertinent to this crucial issue.