We sought to clarify the significance of cardiac dysfunction and to assess its relationship with elevated biomarkers by using cardiovascular magnetic resonance imaging in healthy, middle-aged subjects immediately after they ran 26.2 miles. Cardiac dysfunction and elevated blood markers of myocardial injury have been reported after prolonged strenuous exercise. From 425 volunteers, 13 women and 12 men were randomly selected, provided medical and training history, and underwent baseline cardiopulmonary exercise testing to exhaustion. Blood biomarkers, cardiovascular magnetic resonance imaging, and 24-h ambulatory electrocardiography were performed 4 wk before and immediately after the race. Participants were 38.7+/-9.0 yr old, had baseline peak oxygen consumption of 52.9+/-5.6 ml.kg(-1).min(-1), and completed the marathon in 256.2+/-43.5 min. Cardiac troponin I and B-type natriuretic peptide increased following the race (P=0.001 and P<0.0001, respectively). Cardiovascular magnetic resonance-determined pre- and postmarathon left ventricular ejection fractions were comparable, 57.7+/-4.1% and 58.7+/-4.3%, respectively (P=0.32). Right atrial volume index increased from 46.7+/-14.4 to 57.0+/-14.5 ml/m2 (P<0.0001). Similarly, right ventricular end-systolic volume index increased from 47.4+/-11.2 to 57.0+/-14.6 ml/m2 (P<0.0001) whereas the right ventricular ejection fraction dropped from 53.6+/-7.1 to 45.5+/-8.5% (P<0.0001). There were no morphological changes observed in the left atrium or ventricle or evidence of ischemic injury to any chamber by late gadolinium enhancement. There were no significant arrhythmias. Marathon running causes dilation of the right atrium and right ventricle, reduction of right ventricular ejection fraction, and release of cardiac troponin I and B-type natriuretic peptide but does not appear to result in ischemic injury to any chamber.

Approximately 40% of marathon runners experience a transient rise in serum creatinine that meets criteria of AKI with a parallel elevation of cystatin C, and supportive elevations of neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 in the urine. All biomarker elevations resolved by 24 h. These data suggest that AKI with a transient and minor change in renal filtration function occurs with the stress of marathon running. The impact of repetitive episodes of AKI with long-distance running is unknown.

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Phidippides was a Greek messenger who experienced sudden death after running more than 175 miles in two days. In today's world, marathon running and other endurance sports are becoming more popular and raising concern about sudden deaths at these events. Once etiologies such has hypertrophic cardiomyopathy, anomalous coronary arteries, and coronary atherosclerosis have been excluded, there is now an additional consideration termed Phidippides cardiomyopathy. Because endurance sports call for a sustained increase in cardiac output for several hours, the heart is put into a state of volume overload. It has been shown that approximately one‐third of marathon runners experience dilation of the right atrium and ventricle, have elevations of cardiac troponin and natriuretic peptides, and in a smaller fraction later develop small patches of cardiac fibrosis that are the likely substrate for ventricular tachyarrhythmias and sudden death. Cardiac magnetic resonance imaging is emerging as the diagnostic test of choice for this condition. This review and case report summarizes the key features of this newly appreciated disorder. © 2012 Wiley Periodicals, Inc.The authors have no funding, financial relationships, or conflicts of interest to disclose.

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Background: Invasive fractional flow reserve (FFR INV ) is the standard technique for assessing myocardial ischemia. Pressure distortions and measurement location may influence FFR INV interpretation. We report a technique for performing invasive fractional flow reserve (FFR INV ) by minimizing pressure distortions and identifying the proper location to measure FFR INV . Methods: FFR INV recordings were obtained prospectively during manual hyperemic pullback in 100 normal and diseased coronary arteries with single stenosis, using 4 measurements from the terminal vessel, distal-to-the-lesion, proximal vessel, and guiding catheter. FFR INV profiles were developed by plotting FFR INV values ( y -axis) and site of measurement ( x -axis), stratified by stenosis severity. FFR INV ≤0.8 was considered positive for lesion-specific ischemia. Results: Erroneous FFR INV values were observed in 10% of vessels because of aortic pressure distortion and in 21% because of distal pressure drift; these were corrected by disengagement of the guiding catheter and re-equalization of distal pressure/aortic pressure, respectively. There were significant declines in FFR INV from the proximal to the terminal vessel in normal and stenotic coronary arteries ( P <0.001). The rate of positive FFR INV was 41% when measured from the terminal vessel and 20% when measured distal-to-the-lesion ( P <0.001); 41.5% of positive terminal measurements were reclassified to negative when measured distal-to-the-lesion. Measuring FFR INV 20 to 30 mm distal-to-the-lesion (rather than from the terminal vessel) can reduce errors in measurement and optimize the assessment of lesion-specific ischemia. Conclusions: Meticulous technique (disengagement of the guiding catheter, FFR INV pullback) is required to avoid erroneous FFR INV , which occur in 31% of vessels. Even with optimal technique, FFR INV values are influenced by stenosis severity and the site of pressure measurement. FFR INV values from the terminal vessel may overestimate lesion-specific ischemia, leading to unnecessary revascularization.

This retrospective study was undertaken to assess the responses to, and complications associated with, stress testing in patients with implantable cardioverter-defibrillators (ICDs). Primary end points were occurrence of malignant ventricular arrhythmias, onset of burst pacing or ICD firing, cardiopulmonary resuscitation, or death during or soon after stress testing. Secondary end points were urgent coronary revascularization and/or hospital readmission for cardiovascular complications. During a 4-year period, 1734 patients underwent ICD implantation or generator replacement at our institution; 84 patients (mean age ± SD, 67±12 years; 76% men) subsequently underwent 107 stress tests, including 44 exercise and 63 pharmacologic (22 dobutamine, 41 dipyridamole) evaluations. None of the ICDs were inactivated before testing. All tests were supervised by specially trained paramedical personnel, with a physician immediately available. Four patients had self-terminating, nonsustained ventricular tachycardia at peak stress. None had sustained ventricular tachycardia requiring emergent therapy. There were no deaths or hospital readmissions for ventricular arrhythmias. These findings suggest that stress testing is feasible in patients with ICDs and that it can be performed without pretest inactivation. (Prev Cardiol.