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Effects of cardiac glycosides on atrial fibrillation.

and tricuspid regurgitation, indicative of increased right ventricular stroke volume. A pulmonary-to-systemic flow ratio of 2:1, due to an ostium secundum type-atrial septal defect, could be accurately diagnosed by Doppler echocardiography. Symptoms disappeared sponta-nously within a few minutes after hospital admission without therapy. Laboratory examination revealed elevated serum concentrations of cardiac troponin I (2.2 ng/mL; normal Ͻ 1.6 ng mL) and myocardial band (MB) isoenzyme of creatine kinase (13 U/L; normal Ͻ 5 U/L). MB isoenzyme of creatine kinase peaked (17 U/L) 4 h after hospital admission, and the level of troponin I raised to a peak concentration of 6.4 ng/mL. Other laboratory findings, including inflammatory markers and coagulation tests, were within normal ranges. Coronary angiography showed normal epicardial coronary vessels with no signs of atherosclerotic lesions, and a cineangiogram revealed no wall motion abnormalities. For several reasons, we do not believe that ischemia caused the elevation of cardiac enzymes. First, a normal coronary angiogram finding does not definitely rule out previous coronary artery occlusion, but it makes myocardial ischemia or myocardial infarc-tion unlikely, particularly in the absence of known risk factors for atherosclerosis. 4,5 Second, neither echocardiography nor cinean-giography revealed any wall-motion abnormalities indicative of segmental myocardial damage. Third, elevated concentrations of cardiac troponin have been reported in patients with dilated cardiomyopathy, secondary cardiomyopathies, and acute right ventricular dysfunction. 1,3 To our knowledge, this is the first report in which heavy-resistance exercise induced a raise of levels of serum cardiac troponin and MB isoenzyme of creatine kinase in a patient with preexisting dilatation and dysfunction of the right ventricle due to a ostium secundum type-atrial septal defect with left-to-right shunt. The management of atrial septal defects in older patients is debated persistently, and clinical trials 6,7 have demonstrated conflicting data. We do not have absolute proof to guide our decisions; therefore, we must rely on our experience as well as on the available evidence in deciding how to treat these patients. 8 Further studies are needed to determine whether the management of these patients should be guided by clinical signs or by biochemical markers, like troponins. References 1 Sato Y, Yamada T, Taniguchi R, et al. Serum concentration of cardiac troponin T in patients with cardiomyopathy: a possible mechanism of acute heart failure. Heart 1998; 80:209 – 210 2 Pluim BM, Zwinderman AH, van der Laarse A, et al. The athlete's heart: a meta-analysis of cardiac structure and function. …