Free-Floating Thrombi in the Right Atrium Causing Pulmonary Embolism

A 74-year-old man presented to our Emergency Department with acute dyspnoea. His electrocardiogram showed atrial flutter with 2:1 block and a rate of 150 bpm. Initial investigations revealed a D-dimer level of 6.01 mg/dl. Based on the patient’s complaints and the high D-dimer level, computed tomography pulmonary angiography was immediately performed. This showed no evidence of pulmonary embolism, but there were pneumatic changes in the right upper lung lobe. Antibiotics treatment was started with pipracillin/tazobactam, after which the patient’s condition improved. However, on the third day after admission he developed acute dyspnoea, diaphoresis and cardiopulmonary instability immediately after defecation. To promptly confirm our clinical suspicion of pulmonary embolism, a transthoracic echocardiography was carried out. This demonstrated a worm-like, mobile mass in the right heart. The right ventricle was enlarged, and paradoxical septal motion was present, indicating right ventricular pressure overload. The systolic tricuspid valvular gradient was 56 mmHg. The patient was treated with thrombolysis. His condition was greatly clinically improved after 3 hours. After 10 days of hospitalization, the patient was discharged.

La ateromatosis aórtica aumenta el riesgo de ataque cerebrovascular isquémico

Antecedentes: el ataque cerebrovascular isquémico (ACVi) es causa de mortalidad y discapacidad importante en adultos, siendo la cardioembolia, sobre todo por fibrilación auricular (FA), una etiología importante. Se conocen otras etiologías, cardíacas y no cardíacas, que no siempre pueden definirse, refiriéndose como probables o posibles de cardioaortoembolia. El rol de alguna de ellas, como la ateromatosis aórtica (AA), continúa siendo discutido. Objetivo: analizar fuentes posibles de cardioaortoembolia en pacientes con ACVi reciente. Material y método: estudio caso-control. Se analizaron 100 sujetos con ACVi de menos de 30 días de evolución estudiados prospectivamente con ecocardiograma transesofágico (ETE), entre febrero de 2012 y marzo de 2014. Se apareó cada caso según edad, sexo, presencia de flutter/FA y ausencia de prótesis valvular cardíaca, con un control que se buscó retrospectiva y aleatoriamente entre sujetos con ETE estudiados entre 2010 y 2015 sin ACVi. Se compararon variables binarias mediante test de McNemar y las cuantitativas por test de t pareado; se realizó regresión logística múltiple para ACVi con variables clínicas y hallazgos de ETE y p < 0,1 en el análisis univariado. Se consideró significativo p < 0,05. Variables cuantitativas se expresan en media y desvío estándar (DE) y nominales en valor absoluto y porcentaje, índice de probabilidad (OR) en su valor e intervalo de confianza (IC) 95%. Resultados: se formaron finalmente 76 pares caso-control. Edad casos: 64,3±1,4 y control 64,9±1,3 años (p=0,19); 39 mujeres (51,3%) y 15 sujetos (19,7%) con flutter/FA en cada grupo (p=1). No hubo diferencias significativas según factores de riesgo cardiovascular (FRCV) globales (p=0,06) ni alcoholismo (p=0,80); se encontraron diferencias significativas en la prevalencia de dislipemia (p=0,03) e hipertensión arterial (HTA) (p <0,05). Las indicaciones principales del ETE en los controles fueron: previo a cardioversión eléctrica de FA, sospecha de endocarditis, y valoración de valvulopatía mitral. La ateromatosis aórtica proximal y compleja (AAPC) (p=0,002, OR 5,5, IC95% 1,9-15,9) y la AA en forma global (p=0,001, OR 4,1, IC95% 1,8-9,3), además de la dislipemia (p=0,02, OR 2,8 IC95% 1,2-6,4), se asociaron significativamente con la presencia de ACVi en el análisis multivariado. Conclusión: la AA aumenta significativamente las chances de ACVi y las quintuplica cuando es proximal y compleja. La dislipemia se asoció a ACVi.

Renal and cardiovascular effects of Bothrops marajoensis venom and phospholipase A(2)

Bothrops marajoensis is found in the savannah of Marajo Island in the State of Par S and regions of Amapa State, Brazil. The aim of the work was to study the renal and cardiovascular effects of the B. marajoensis venom and phospholipase A(2) (PLA(2)). The venom was fractionated by Protein Pack 5PW. N-terminal amino acid sequencing of sPLA(2) showed amino acid identity with other lysine K49sPLA(2)s of snake venom. B. marajoensis venom (30 mu g/mL) decreased the perfusion pressure, renal vascular resistance, urinary flow, glomerular filtration rate and sodium tubular transport. PLA(2) did not change the renal parameters. The perfusion pressure of the mesenteric bed did not change after infusion of venom. In isolated heart, the venom decreased the force of contraction and increased PP but did not change coronary flow. In the arterial pressure, the venom and PLA(2) decreased mean arterial pressure and cardiac frequency. The presence of atrial flutter and late hyperpolarisation reversed, indicating QRS complex arrhythmia and dysfunction in atrial conduction. In conclusion, B. marajoensis venom and PLA(2) induce hypotension and bradycardia while simultaneously blocking electrical conduction in the heart. Moreover, the decrease in glomerular filtration rate, urinary flow and electrolyte transport demonstrates physiological changes to the renal system. (C) 2009 Elsevier Ltd. All rights reserved.

Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013

Background: Up-to-date evidence on levels and trends for age-sex-specific all-cause and cause-specific mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries. Methods We estimated age-sex-specific all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specific causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-country-year group to sum to all-cause mortality based on draws from the uncertainty distributions. Findings Global life expectancy for both sexes increased from 65·3 years (UI 65·0-65·6) in 1990, to 71·5 years (UI 71·0-71·9) in 2013, while the number of deaths increased from 47·5 million (UI 46·8-48·2) to 54·9 million (UI 53·6-56·3) over the same interval. Global progress masked variation by age and sex: for children, average absolute differences between countries decreased but relative differences increased.For women aged 25-39 years and older than 75 years and for men aged 20-49 years and 65 years and older, both absolute and relative differences increased. Decomposition of global and regional life expectancy showed the prominent role of reductions in age-standardised death rates for cardiovascular diseases and cancers in high-income regions, and reductions in child deaths from diarrhoea, lower respiratory infections, and neonatal causes in low-income regions. HIV/AIDS reduced life expectancy in southern sub-Saharan Africa. For most communicable causes of death both numbers of deaths and age-standardised death rates fell whereas for most non-communicable causes, demographic shifts have increased numbers of deaths but decreased age-standardised death rates. Global deaths from injury increased by 10·7%, from 4·3 million deaths in 1990 to 4·8 million in 2013; but age-standardised rates declined over the same period by 21%. For some causes of more than 100 000 deaths per year in 2013, age-standardised death rates increased between 1990 and 2013, including HIV/AIDS, pancreatic cancer, atrial fibrillation and flutter, drug use disorders, diabetes, chronic kidney disease, and sickle-cell anaemias. Diarrhoeal diseases, lower respiratory infections, neonatal causes, and malaria are still in the top five causes of death in children younger than 5 years. The most important pathogens are rotavirus for diarrhoea and pneumococcus for lower respiratory infections. Country-specific probabilities of death over three phases of life were substantially varied between and within regions. Interpretation For most countries, the general pattern of reductions in age-sex specific mortality has been associated with a progressive shift towards a larger share of the remaining deaths caused by non-communicable disease and injuries. Assessing epidemiological convergence across countries depends on whether an absolute or relative measure of inequality is used. Nevertheless, age-standardised death rates for seven substantial causes are increasing, suggesting the potential for reversals in some countries. Important gaps exist in the empirical data for cause of death estimates for some countries; for example, no national data for India are available for the past decade.

Experimentally and coupled CFD/CSD assisted structural and aeroelastic modelling of the Javelin UAV outboard wing section

This study presents the procedure followed to make a prediction of the critical flutter speed for a composite UAV wing. At the beginning of the study, there was no information available on the materials used for the construction of the wing, and the wing internal structure was unknown. Ground vibration tests were performed in order to detect the structure’s natural frequencies and mode shapes. From tests, it was found that the wing possesses a high stiffness, presenting well separated first bending and torsional natural frequencies. Two finite element models were developed and matched to experimental results. It has been necessary to introduce some assumptions, due to the uncertainties regarding the structure. The matching process was based on natural frequencies’ sensitivity with respect to a change in the mechanical properties of the materials. Once experimental results were met, average material properties were also found. Aerodynamic coefficients for the wing were obtained by means of a CFD software. The same analysis was also conducted when the wing is deformed in its first four mode shapes. A first approximation for flutter critical speed was made with the classical V - g technique. Finally, wing’s aeroelastic behavior was simulated using a coupled CFD/CSD method, obtaining a more accurate flutter prediction. The CSD solver is based on the time integration of modal dynamic equations, requiring the extraction of mode shapes from the previously performed finite-element analysis. Results show that flutter onset is not a risk for the UAV, occurring at velocities well beyond its operative range.

Interatrial block and atrial arrhythmias in centenarians: Prevalence, associations, and clinical implications

Data are lacking on the characteristics of atrial activity in centenarians, including interatrial block (IAB). The aim of this study was to describe the prevalence of IAB and auricular arrhythmias in subjects older than 100 years and to elucidate their clinical implications. We studied 80 centenarians (mean age 101.4 ± 1.5 years; 21 men) with follow-ups of 6–34 months. Of these 80 centenarians, 71 subjects (88.8%) underwent echocardiography. The control group comprised 269 septuagenarians. A total of 23 subjects (28.8%) had normal P wave, 16 (20%) had partial IAB, 21 (26%) had advanced IAB, and 20 (25.0%) had atrial fibrillation/flutter. The IAB groups exhibited premature atrial beats more frequently than did the normal P wave group (35.1% vs 17.4%; P < .001); also, other measurements in the IAB groups frequently fell between values observed in the normal P wave and the atrial fibrillation/flutter groups. These measurements included sex preponderance, mental status and dementia, perceived health status, significant mitral regurgitation, and mortality. The IAB group had a higher previous stroke rate (24.3%) than did other groups. Compared with septuagenarians, centenarians less frequently presented a normal P wave (28.8% vs 53.5%) and more frequently presented advanced IAB (26.3% vs 8.2%), atrial fibrillation/flutter (25.0% vs 10.0%), and premature atrial beats (28.3 vs 7.0%) (P < .01). Relatively few centenarians (<30%) had a normal P wave, and nearly half had IAB. Our data suggested that IAB, particularly advanced IAB, is a pre–atrial fibrillation condition associated with premature atrial beats. Atrial arrhythmias and IAB occurred more frequently in centenarians than in septuagenarians.

Cavotricuspid isthmus: anatomy and electrophysiology features: its evaluation before radiofrequency ablation

The cavotricuspid isthmus (CTI) in the lower pan of the right atrium, between the inferior caval vein and the tricuspid valve, is considered crucial in producing a conduction delay and. hence, favoring the perpetuation of a reentrant circuit. Non-uniform wall thickness, muscle fiber orientation and the marked variability in muscular architecture in the CTI should be taken into consideration from the perspective of anisotropic conduction, thus producing an electrophysiologic isthmus. The purpose of this article is to review the anatomy and electrophysiology of the CTI in human hearts to provide useful information to plan CTI radio frequency ablation for the patients with atrial flutter.