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.

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.

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.

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.