The Role of Cardiovascular Magnetic Resonance in Sports Cardiology; Current Utility and Future Perspectives.

Cardiovascular magnetic resonance (CMR) is frequently used in the investigation of suspected cardiac disease in athletes. In this review, we discuss how CMR can be used in athletes with suspected cardiomyopathy with particular reference to volumetric analysis and tissue characterization. We also discuss the finding of non-ischaemic fibrosis in athletes describing its prevalence, distribution and clinical importance.The strengths of CMR include high spatial resolution, unrestricted imaging planes and lack of ionizing radiation. Regular physical exercise leads to cardiac remodeling that in certain situations can be clinically challenging to differentiate from various cardiomyopathies. Thorough morphological assessment by CMR is fundamental to ensuring accurate diagnosis. Developments in tissue characterization by late gadolinium enhancement and T1 mapping have the potential to be powerful additional tools in this challenging clinical situation. Using late gadolinium enhancement, it is also possible to detect non-ischaemic fibrosis in athletes who do not have overt cardiomyopathy. The mechanisms of this fibrosis are unclear; however, it does appear to be clinically important. We also review data on the prevalence of non-ischaemic fibrosis in athletes. CMR is a powerful tool to aid in the diagnosis of cardiomyopathy in athletes. It may also have a future role in assessing fibrosis related to long-term participation in sport

Induction of Atrial Fibrillation by Neutrophils Critically Depends on CD11b/CD18 Integrins

Background: Recent observational clinical and ex-vivo studies suggest that inflammation and in particular leukocyte activation predisposes to atrial fibrillation (AF). However, whether local binding and extravasation of leukocytes into atrial myocardium is an essential prerequisite for the initiation and propagation of AF remains elusive. Here we investigated the role of atrial CD11b/CD18 mediated infiltration of polymorphonuclear neutrophils (PMN) for the susceptibility to AF. Methods and Results: C57bl/6J wildtype (WT) and CD11b/CD18 knock-out (CD11b(-/-)) mice were treated for 14 days with subcutaneous infusion of angiotensin II (Ang II), a known stimulus for PMN activation. Atria of Ang II-treated WT mice were characterized by increased PMN infiltration assessed in immunohistochemically stained sections. In contrast, atrial sections of CD11b(-/-) mice lacked a significant increase in PMN infiltration upon Ang II infusion. PMN infiltration was accompanied by profoundly enhanced atrial fibrosis in Ang II treated WT as compared to CD11b(-/-) mice. Upon in-vivo electrophysiological investigation, Ang II treatment significantly elevated the susceptibility for AF in WT mice if compared to vehicle treated animals given an increased number and increased duration of AF episodes. In contrast, animals deficient of CD11b/CD18 were entirely protected from AF induction. Likewise, epicardial activation mapping revealed decreased electrical conduction velocity in atria of Ang II treated WT mice, which was preserved in CD11b(-/-) mice. In addition, atrial PMN infiltration was enhanced in atrial appendage sections of patients with persistent AF as compared to patients without AF. Conclusions: The current data critically link CD11b-integrin mediated atrial PMN infiltration to the formation of fibrosis, which promotes the initiation and propagation of AF. These findings not only reveal a mechanistic role of leukocytes in AF but also point towards a potential novel avenue of treatment in AF