Magnitude, reproducibility, and association with baseline cardiac function of cardiac biomarker release in long-distance runners aged > or =55 years.

Cardiac biomarker release after endurance exercise has been described in young athletes. Although older athletes are increasingly active in such sports, they have not previously been studied. Therefore, the aim of this study was to assess the magnitude and reproducibility of biomarker release in athletes aged > or =55 years. Forty-three healthy athletes (mean age 61 +/- 3.6 years) were assessed before and immediately after a 30-km cross-country race and studied with echocardiography at rest. The median N-terminal pro-brain natriuretic peptide (NT-proBNP; normal <194 ng/L) level was 42 ng/L (interquartile range 30 to 95) at baseline and 191 ng/L (interquartile range 114 to 308) after the race. Troponin T (normal <0.03 microg/L) was elevated in 19 subjects (44%) after the race. Twenty-two subjects had also been studied 3 years before at the same race, using an identical test protocol. Between the 2 races, strong correlations were seen for individual runners' postrace biomarker levels (NT-proBNP: r = 0.82, log transformed data; troponin T: Spearman's rho = 0.84; p <0.001 for both). The coefficient of variation for NT-proBNP release was 8.1%. Levels of NT-proBNP after the race were correlated with levels at baseline (r = 0.93, p <0.001) and with left ventricular mass index (r = 0.32, p = 0.03). Moreover, participants with elevated postrace NT-proBNP were significantly older (62.0 vs 59.8 years, p = 0.04). In conclusion, long-distance runners aged > or =55 years released NT-proBNP and troponin T in a reproducible fashion. The magnitude of NT-proBNP release during the race was correlated strongly with NT-proBNP baseline levels and was associated with left ventricular mass and age. These findings may suggest a potential adverse effect of long-distance running on cardiac function in certain participants in this age group.

[Rheumatic heart disease behind life-threatening heart failure in pregnancy]. / Reumatisk hjärtsjukdom bakom livshotande hjärtsvikt hos gravid.

Valvular heart disease constitutes the majority of all causes of heart disease in pregnancy. In the presence of valvular heart disease, the necessary haemodynamic changes of pregnancy might cause heart failure, leading to severe maternal and fetal morbidity and even mortality. In lower-income countries, rheumatic heart disease remains one of the major causes of death related to pregnancy [6]. In low-income countries, rheumatic heart disease is found in 60% to 80% of the pregnant women with heart disease, and 10% to 30% have a congenital disorder including congenital valve disorders [4]. The most common valvular lesion of rheumatic heart disease is mitral stenosis. This valvular lesion can be the cause of extreme disability and even mortality during pregnancy due to an increase in the transvalvular gradient and a rise in left atrial pressure. The maternal mortality associated with mitral stenosis is stratified by New York Heart Association (NYHA) classification: class I, 0.1%; class II, 0.3%; class III, 5.5%; and class IV, 6.0%. Most patients are in class I or II at presentation, but 12% to 25% of patients are in class III or IV [14].

Cardiac fatigue in long-distance runners is associated with ventricular repolarization abnormalities.

BACKGROUND: Prolonged exercise can induce cardiac fatigue, which is characterized by biomarker release and impaired myocardial function. The impact on ventricular electrophysiology is largely unknown. OBJECTIVE: The objective of this study was to examine changes in ventricular repolarization after a 30-km cross-country race in runners aged >or=55 years. METHODS: Fifteen healthy participants (62 +/- 5 years) were assessed using biomarkers (N-terminal pro-brain natriuretic peptide [NT-proBNP], troponin T [TnT]), tissue Doppler echocardiography, and vectorcardiography at baseline, within 1 hour postrace and on days 1 and 6 postrace. RESULTS: During the race, NT-proBNP increased from 42 ng/L (interquartile range 25-117) to 187 ng/L (113-464), and TnT increased from undetectable levels to 0.03 microg/L (0.015-0.05). Global strain (19.1% +/- 2.2%) decreased on day 1 (17.2% +/- 1.8%) and day 6 (17.9% +/- 1.5%; P <.01). QT(c) increased from 431 +/- 15 ms prerace to 445 +/- 22 ms postrace and 445 +/- 15 ms on day 1 (P <.05), mainly because of an increased T(peak-end) interval (prerace 108 +/- 13 ms, postrace 127 +/- 43 ms, day 1 127 +/- 43 ms; P <.05). Postrace, T(area) (baseline 75 +/- 26 microVs) peaked on day 1 (105 +/- 42 microVs) and remained high on day 6 (89 +/- 37 microVs; P <.05). Runners with higher baseline NT-proBNP developed greater impairment of myocardial velocities (rho = -0.68 to -0.54; P <.05) and a larger increase in T(area) (rho = 0.73; P <.01). CONCLUSION: Cardiac fatigue induced by prolonged exertion is associated with sustained abnormalities in ventricular repolarization. Runners with higher baseline NT-proBNP are especially liable to such alterations of cardiac function.