No cardiac damage after endurance exercise in cardiologists cycling to the European Society of Cardiology meeting in Barcelona.

AIMS: There are variable results reported for athletes and potential cardiac damage during exercise. In 2009 a group of cardiologists went by bicycle from the Netherlands to the European Society of Cardiology meeting in Barcelona and collected functional and biochemical parameters during this trip in order to evaluate whether cardiac damage was observed in a group of moderately trained amateur cyclists. METHODS AND RESULTS: All of the 20 amateur cyclists (17 men) completed the 1580 km in eight days with an average speed of 27.9 km and an average distance of 190 km/day. Cardiac damage was predefined as wall motion abnormalities detected by echocardiography or an increase of troponin I exceeding three times the upper limit. Although skeletal muscle damage was found in all of the cyclists, no cardiac damage could be detected. CONCLUSION: This long distance bicycle trip performed by moderately trained cardiologists demonstrates that it was safe and feasible and did not lead to cardiac damage although skeletal muscle damage was demonstrated in all participants.

Rapidly rule out acute myocardial infarction by combining copeptin and heart-type fatty acid-binding protein with cardiac troponin.

BACKGROUND: The rapid exclusion of acute myocardial infarction in patients with chest pain can reduce the length of hospital admission, prevent unnecessary diagnostic work-up and reduce the burden on our health-care systems. The combined use of biomarkers that are associated with different pathophysiological aspects of acute myocardial infarction could improve the early diagnostic assessment of patients presenting with chest pain. METHODS: We measured cardiac troponin I, copeptin and heart-type fatty acid-binding protein concentrations in 584 patients who presented to the emergency department with acute chest pain. The diagnostic performances for the diagnosis of acute myocardial infarction and NSTEMI were calculated for the individual markers and their combinations. Separate calculations were made for patients presenting to the emergency department <3 h, 3-6 h and 6-12 h after chest pain onset. RESULTS: For ruling out acute myocardial infarction, the net predictive values (95% CI) of cardiac troponin I, copeptin and heart-type fatty acid-binding protein were 90.4% (87.3-92.9), 84% (79.8-87.6) and 87% (83.5-90), respectively. Combining the three biomarkers resulted in a net predictive value of 95.8% (92.8-97.8). The improvement was most pronounced in the early presenters (<3 h) where the combined net predictive value was 92.9% (87.3-96.5) compared to 84.6% (79.4-88.9) for cardiac troponin I alone. The area under the receiver operating characteristic for the triple biomarker combination increased significantly (P < 0.05) compared to that of cardiac troponin I alone (0.880 [0.833-0.928] vs. 0.840 [0.781-0.898], respectively). CONCLUSIONS: Combining copeptin, heart-type fatty acid-binding protein and cardiac troponin I measurements improves the diagnostic performance in patients presenting with chest pain. Importantly, in patients who present early (<3 h) after chest pain onset, the combination improves the diagnostic performance compared to the standard cardiac troponin I measurement alone.

Development of contractile dysfunction in rat heart failure: hierarchy of cellular events.

The cellular mechanisms underlying the development of congestive heart failure (HF) are not well understood. Accordingly, we studied myocardial function in isolated right ventricular trabeculae from rats in which HF was induced by left ventricular myocardial infarction (MI). Both early-stage (12 wk post-MI; E-pMI) and late, end-stage HF (28 wk post-Mi; L-pMI) were studied. HF was associated with decreased sarcoplasmic reticulum Ca(2+) ATPase protein levels (28% E-pMI; 52% L-pMI). HF affected neither sodium/calcium exchange, ryanodine receptor, nor phospholamban protein levels. Twitch force at saturating extracellular [Ca(2+)] was depressed in HF (30% E-pMI; 38% L-pMI), concomitant with a marked increase in sensitivity of twitch force toward extracellular [Ca(2+)] (26% E-pMI; 68% L-pMI). Ca(2+)-saturated myofilament force development in skinned trabeculae was unchanged in E-pMI but significantly depressed in L-pMI (45%). Tension-dependent ATP hydrolysis rate was depressed in L-pMI (49%), but not in E-pMI. Our results suggest a hierarchy of cellular events during the development of HF, starting with altered calcium homeostasis during the early phase followed by myofilament dysfunction at end-stage HF.