Articles

Introduction: Cardiovascular diseases are the leading cause of death in the world, headed by coronary artery disease, which is secondary to atherosclerosis. The latter recognizes classic risk factors such as diabetes, high blood pressure, tobacco, and dyslipidemia and other less classic factors such as chronic inflammation of rheumatoid arthritis. Many studies have highlighted the correlation between this chronic inflammation and clinical coronary disease but very few have focused on the anatomical correlation. Objective: To describe the correlation between the chronic biological inflammation of rheumatoid arthritis and anatomical coronary lesions on angiography. Method: This observational, retrospective, single-center study, including over 10 years, of patients with rheumatoid arthritis, confirmed the EULAR 2010 criteria and presented with coronary artery disease requiring coronary angiography. Patients with missing data or in whom coronary angiography was not done were excluded (n = 14). We divided then the patients according to the existence or not of chronic inflammation to study the impact of the latter on the existence (Stenosis < 50% vs. stenosis ≥ 50%), the extent (single vs. multivessel disease), and the severity of the coronary lesions (syntax score < 32 vs. ≥ 32). Results: 202 patients (49♂/153♀) aged between 30-75 years with a history of rheumatoid arthritis have had a coronary event requiring coronary angiography, were included; The mean ejection fraction at baseline was 57.3% +/- 5.8 (37 vs.-65%). 75% of them were ≥ 65 years old. 55% were diabetics, 61% with hypertension, 38% with dyslipidemia, and 19% were smokers. Chronic inflammation was diagnosed in 70% of them on non-specific parameters (ESR, CRP, fibrinogen, anemia, and rheumatoid factor). All patients had coronary angiography, which made it possible to identify the coronary lesions according to their existence (Stenosis < 50%: 51 patients vs. stenosis ≥ 50%: 151 patients), the extent (single: 86 patients vs. multivessel disease: 116 patients) and the severity of the coronary lesions (syntax score < 32: 142 patients vs. ≥ 32: 60 patients). Chronic inflammation of rheumatoid arthritis was correlated in bivariate and multivariate analysis (after excluding the impact of other risk factors) with the existence and extent of coronary lesions (p < 0.05) but not with their severity (p > 0.05). Discussion: The two limitations of this work are the monocentric nature of the study and the absence of specific inflammatory parameters such as anti-CCP antibodies. Strengths are anatomical correlations and multivariate analysis. Chronic inflammation apart from any influence of the various risk factors predisposes to the existence and extent of coronary lesions (p < 0.05). The severity of coronary lesions assessed by Syntax Score was not correlated with chronic inflammation, although other studies suggest that this inflammation is the cause of complex lesions.Interpretation: Rheumatoid arthritis is associated with an increase in cardiac morbidity and mortality. Atheromatous lesions are more frequent in those patients than the existence of classic cardiovascular risk factors would suggest. Several explanations could account for this risk: the inflammatory syndrome and its impact on the cardiovascular risk factors and the vessel and the deleterious effect of the treatments. This requires stricter screening and management of risk factors in rheumatoid arthritis.

Introduction: Atrial Septal Defect (ASD) is the most common congenital heart disease, accessible to percutaneous closure in 90% of cases. The closure procedure is performed usually under local anesthesia and TTE by femoral access. The association of OS-ASD with an azygos continuation of the inferior vena cava is very rare (< 0.1/1000 births) making femoral access impossible. Only a few cases are mentioned in the literature, here we describe the procedure as faithfully as possible. Important clinical finding: We present a case of a 32-years-old female candidate for percutaneous closure of OS-ASD with right cavity dilatation who present during her procedure an unusual guidewire path suspecting an azygos continuation of the inferior vena cava, confirmed by CT angiography, making impossible the closure via the femoral approach. Therapeutic intervention: After being confronted with the categorical patient refusal of the surgery, we performed successfully the procedure; one month later; under general sedation by internal jugular approach. We finished with manual compression before extubating the patient. Outcomes: The follow-up was favorable at the cost of a hematoma at the puncture site and brachial plexus compression, which regressed after 3 days. Conclusion: We opted for general anesthesia and intubation to guide the procedure by TEE. We placed it in the aorta, which gave us good stability to continue successfully the procedure. We underestimated the risk of complication at the puncture site, which could have been avoided by using a vascular suture device or more prolonged compression. Main takeaway lesson: Percutaneous closure is the reference treatment for OS-ASD. In case of is associated with an azygos continuation of the inferior vena cava, the right internal jugular vein remains a reasonable approach; it requires discussion and rigorous preparation by the whole team. The management of the puncture site in this situation remains delicate and requires great concentration. 

Percutaneous coronary angioplasty is a minimally invasive procedure aimed at unclogging a coronary artery with a low complication rate (with a serious complication rate of 3% to 7% and a mortality rate of 1.2%). Device entrapment during PCI is a rare but life-threatening complication that occurs in < 1% of PCIs and balloon entrapment comes second after coronary guidewires. We present the case of 68-years-old man, smoker, hypertensive and type2 diabetic that presents angina with evidence of ischemia on myocardial tomoscintigraphy and in whom the radial coronary angiography reveals a tight calcified mid LAD stenosis. During his PCI and after dilatation with an NC balloon 2.5 × 12 the latter refuses to deflate and remains trapped in the lesion with the appearance of pain and ST-elevation despite several attempts to dilute the product in the inflator and to burst it by overexpansion. Traction on the balloon resulted in the deep intubation of the guiding-catheter, which comes in contact with the trapped balloon, and the rupture of the latter’s hypotube, which remains inflated at the site of the lesion and mounted on the 0.014 guidewire. We put a second 0.014 guidewire distally in the LAD and twisted with the distal part of the first guidewire, then we introduced a second balloon 2.0 × 20 over the second guidewire until the distal part of the guiding-catheter and inflated to trap the stucked balloon. We gradually removed this emergency assembly that allowed us to retrieve the trapped balloon. The control injection revealed a thrombotic occlusion of the LAD treated by thrombectomy and anti-GPIIbIIIa followed by a DES 2.75 × 28 placement. The patient was discharged 48 hours later with a good LVEF. The possible balloon entrapment mechanisms are an acute recoil of a highly calcified lesion with compression of the incompletely deflated balloon, which seems to be the case in our patient, strangulation of the proximal balloon end by the guiding-catheter if the balloon is removed before complete deflation and break or bend of the hypotube. The solutions in case of undeflatable balloon entrapment are to dilute the product in the inflator, to burst it by overexpansion, to pierce it through a stiff guidewire (or through its other end on a Microcatheter or OTW balloon), to cut its outer part and let it empty passively, to introduce a second guide-wire and perform a Buddy-Balloon or to transfer the patient to Surgery. Material entrapment remains a rare but life-threatening complication, its eviction requires the choice of material size and gentle manipulations (small balloons in the event of a calcified lesion) and its management uses different techniques, the choice of which depends on the clinical and anatomical situation. 

Specific quantification of therapeutic tissue stem cells (TSCs) is a major challenge. We recently described a computational simulation method for accurate and specific counting of TSCs. The method quantifies TSCs based on their unique asymmetric cell kinetics, which is rate-limiting for TSCs’ production of transiently-amplifying lineage-committed cells and terminally arrested cells during serial cell culture. Because of this basis, the new method is called kinetic stem cell (KSC) counting. Here, we report further validations of the specificity and clinical utility of KSC counting. First, we demonstrate its quantification of the expected increase in the hematopoietic stem cell (HSC) fraction of CD34+-selected preparations of human-mobilized peripheral blood cells, an approved treatment product routinely used for HSC transplantation therapies. Previously, we also used the KSC counting technology to define new mathematical algorithms with the potential for rapid determination of TSC-specific fractions without the need for serial culture. A second important HSC transplantation treatment, CD34+-selected umbilical cord blood (UCB) cells, was used to investigate this prediction. We show that, with an input of only simple population doubling time (PDT) data, the KSC counting-derived “Rabbit algorithms” can be used to rapidly determine the specific HSC fraction of CD34+-selected UCB cell preparations with a high degree of statistical confidence. The algorithms define the stem cell fraction half-life (SCFHL), a new parameter that projects stem cell numbers during expansion culture. These findings further validate KSC counting’s potential to meet the long-standing unmet need for a method to determine stem cell-specific dosage in stem cell medicine.

Pulmonary edema is a rare but potentially life-threatening iatrogenic complication after treatment through therapeutic thoracentesis of a collapsed lung due to a hydro- or pneumo-thorax. 

Thousands of tons of biodegradable organic waste generates in urban and rural areas every day, creating disposal problems. Urban organic waste can be converted into valuable output products (vermicompost, vermin-liquid, and earthworms) by applying a vermicomposting technique that had different. Implementing green roofs via soilless culture systems as micro-scale farms led to increasing natural resource use efficiencies as well as producing fresh food. The integration of both techniques will create not just reduce pollution and climate change impacts but also for increasing food production and security in urban, enhance the lifestyle and increase public awareness of environmental issues. This process is profitable at any scale of operation.

Smart agriculture applications (monitoring, sensing, automation and control) of micro-climate and environmental conditions for different agriculture production sectors and scales, decision-makers and researchers need to take it into consideration to strengthen the efforts of mitigation and adaption of climate change impacts as well as maximize the natural resources use efficiencies and food production. Motivate the farmers to implement smart agriculture applications, especially in developed and poor countries, strong cooperation for technology transfer and build up the technology infrastructure of information and communication (ICT) plus the internet of things (IoT).

Approximately 73.4% of global deaths are caused by chronic non-communicable diseases, among them, cardiovascular and cerebrovascular diseases, tumors, and chronic respiratory diseases ranked in the top 3 respectively [1]. An accumulating body of evidence showed that the risk of all-cause mortality in cancer patients with cardiovascular disease (CVD) was 3.78 times higher than that of those without CVD and 8.8% of cancer survivors died of CVD [2]. Heart failure (HF) is a serious manifestation or terminal stage of various heart diseases. Although myocardial damage and dysfunction are the main causes of HF, the cardiovascular injury caused by the tumor itself and the detrimental effect of cancer treatment also play an important role. More recently, the data has suggested that up to 25% - 30% of patients with HF have histories of cancer for about 10 years; and cancer also determines the prognosis of heart HF [3]. 

Multiple Sclerosis (MS) is a chronic and often progressive condition that affects the Central Nervous System (CNS) and as a result has negative consequences on a person’s physical condition, functioning, mood, and Activities of Daily Living (ADL) [1]. 

The impact of culture on the communication of pain becomes visible in a comparative perspective when individuals with two different cultures meet.Regardless of the physiological cause, it is through lived experience, in social life, that it is decided how, where, when and for whom pain is to be communicated. Age and gender, situation and context as well as the type of pain are essential ingredients in communication. The communication is always adapted to expectations from those present, their own experiences of pain and the specific circumstances, the cause of the pain. The impact of culture on the communication of pain becomes visible in a comparative perspective when individuals with two different cultures meet.