Association between exposure to air pollution and incidence of atrial fibrillation.

INTRODUCTION AND OBJECTIVE: Air pollution is the largest environmental health risk, estimated to cause over 5 million premature deaths per year worldwide, including half million deaths in Europe. It is associated with significant reductions in healthy life years and worker productivity. It may also be an important endocrine disrupter, contributing to the development of metabolic diseases such as obesity and diabetes mellitus and due to acute ischaemic/thrombotic cardiovascular events. Aim of the study was to present the current knowledge on short- and long-term exposure to air pollution, including particulate matter (PM2.5 and PM10) and the occurrence of atrial fibrillation (AF). REVIEW METHODS: The review article was based on data obtained from articles published in the PubMed or related databases. We searched observational studies. ABBREVIATED DESCRIPTION OF THE STATE OF KNOWLEDGE: Some of the studies demonstrated a triggering effect of exposure to air pollution on acute exacerbation of atrial fibrillation. Evidence for a long-term effect of air pollution exposure on AF episodes is even more scarce or limited. SUMMARY: Data indicate that human exposure to air pollution is associated with an increased risk of atrial fibrillation. Studies confirmed that further efforts to reduce air pollution exposure should be undertaken to reduce the negative health effects in the general population. To better understand the effect of air pollution on incidence of AF and the related public health impact in the most polluted regions of the world, more high-quality studies are needed.

Distances between transseptal puncture site and anatomical landmarks.

The aim of the study was to provide quantitative data and to look for new landmarks useful during transseptal puncture (TSP) using a fluoroscopy-guided approach. METHODS AND RESULTS: A total of 104 patients at mean age 57 ± 12 years, of whom 92% underwent pulmonary vein isolation, were analysed. Before TSP catheters were placed in the coronary sinus (CS) and His bundle region. A guidewire running from femoral vein through great veins was left loose in superior vena cava. Before TSP X-ray images were taken in right anterior oblique (RAO) 45° and RAO 53° projections. Locations posterior to TSP site in RAO were described with negative values and those anterior with positive values. The measured distances in millimeters were as follows: (a) between TSP site and posterior atrial wall (RAO 45 = -21 ± 7 mm; RAO 53 = -19 ± 6 mm (b) between TSP site and free guidewire (RAO 45 = -5 ± 4 mm, RAO 53 = -3 ± 4 mm (c) between TSP site and CS ostium (RAO 45 = 9 ± 6 mm; RAO 53 = 8 ± 5 mm (d) between TSP site and His region (RAO 45 = 29 ± 8 mm; RAO 53 = 30 ± 8 mm). We observed correlations between measured distances and age, body mass index and sizes of cardiac chambers. The distance between TSP site and the line projected by the guidewire running between great veins, measured in mid-RAO projections, was very small. CONCLUSION: The distances between TSP site and standard anatomical landmarks used during TSP vary with regard to age, physique and cardiac chamber dimensions. TSP site, as assessed in mid RAO, is in direct vicinity to the line projected by a guidewire running between the great veins.

[Is Q-wave on admission associated with microvascular injury in patients with acute myocardial infarction treated with primary angioplasty?]. / Czy obecnosc patologicznego zalamka Q przy przyjeciu predysponuje do poreperfuzyjnego uszkodzenia mikrokrazenia u pacjentów ze swiezym zawalem miesnia sercowego, leczonych pierwotna angioplastyka wiencowa?

INTRODUCTION: Impaired microvascular flow, despite patent epicardial artery (no-reflow phenomenon), leads to greater left ventricular dysfunction after myocardial infarction (MI). Predictive factors associated with no-reflow remain largely unexplored. Q-wave on admission (Q(A)) is a sign of extensive ischemia probably predisposing to no-reflow. The aim of the study was to explore possible relation between Q(A) and electrocardiographic signs of no-reflow in patients with first MI. MATERIAL AND METHODS: The study group was composed of 108 patients (81 men; mean age 60+/-11 years), with first ST-segment elevation MI, treated successfully with primary angioplasty (p-PTCA). ECG tracings were obtained before and 30 minutes after p-PTCA. The sum of ST-segment elevations (sum(ST(el))) in 3 contiguous leads with the highest ST(el) was calculated. Lack of 50% reduction of the sum(ST(el)) 30 minutes after angioplasty was defined as ECG sign of no-reflow. Presence of Q(A) was estimated in leads with ST(el). RESULTS: Q(A) was found in 42 (39%) patients. Q(A) was more often observed in patients with ECG signs of no-reflow (38% vs. 18%; p<0.05). Group with Q(A) showed larger damage of left ventricle estimated with ECG QRS score (7.7+/-4.4 vs. 6.1+/-3.4; p<0.05) as well as worse ejection fraction (42% vs. 46%; p=0.05). CONCLUSIONS: Patients with Q(A) have more often ECG signs of no-reflow than other patients with MI. Previously described worse function of left ventricle in this group, may be partially caused by more frequent no-reflow occurring in those patients. This fact suggests that adjunctive therapy preventing no-reflow could be beneficial in this group of patients.