RESUMO
Atrial fibrillation (AF) is the most common sustained heart rhythm disorder and is often associated with symptoms that can significantly impact quality of life and daily functioning. Palpitations are the cardinal symptom of AF and many AF therapies are targeted towards relieving this symptom. However, up to two-third of patients also complain of dyspnea as a predominant self-reported symptom. In clinical practice it is often challenging to ascertain whether dyspnea represents an AF-related symptom or a symptom of concomitant cardiovascular and non-cardiovascular comorbidities, since common AF comorbidities such as heart failure and chronic obstructive pulmonary disease share similar symptoms. In addition, therapeutic approaches specifically targeting dyspnea have not been well validated. Thus, assessing and treating dyspnea can be difficult. This review describes the latest knowledge on the burden and pathophysiology of dyspnea in AF patients. We discuss the role of heart rhythm control interventions as well as the management of AF risk factors and comorbidities with the goal to achieve maximal relief of dyspnea. Given the different and often complex mechanistic pathways leading to dyspnea, dyspneic AF patients will likely profit from an integrated multidisciplinary approach to tackle all factors and mechanisms involved. Therefore, we propose an interdisciplinary and integrated care pathway for the work-up of dyspnea in AF patients.
RESUMO
BACKGROUND: Immunoglobulin κ and λ free light chains (FLC) are important serum biomarkers for diagnosing and monitoring plasma cell dyscrasias (via the κ:λ FLC ratio), and assessing immune competence and activation status (via ∑FLC). FLCs are produced, in excess of heavy chains, from healthy plasma cells during immunoglobulin production, but unlike intact immunoglobulins that are cleared by cellular catabolism over a number of weeks, FLC are rapidly cleared from the bloodstream by the renal glomerulus with a half-life of 3 (κ FLC)-6 (λ FLC) hours. Marathon running has been shown to acutely and transiently decrease renal function, however, the impact of prolonged aerobic exercise on FLC levels remains unknown. METHODS: We measured serum FLC levels in 60 runners before, and immediately after, the 2010 Eindhoven Marathon. RESULTS: A significant increase (p<0.01) in κ FLC levels was observed after the marathon, and κ FLC correlated positively with serum creatinine levels. No changes were observed for λ FLC, and thus, there were subtle elevations in the ∑FLC and FLC ratio in some participants. Indeed, we found that 13% of participants had an abnormally increased FLC ratio upon completion of the marathon; a phenomenon previously observed in renal diseases. CONCLUSIONS: Abnormal FLC ratios observed after exercise reflected an increase in serum κ FLC levels, which may be due to acute and transient reductions in renal function during exercise, though we also observed an increase in serum IgG and IgA and thus cannot exclude exercise-induced immune stimulation or immunoglobulin redistribution.