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.