We evaluated the influence of a 14-wk endurance running program on the exercise-induced release of high-sensitivity cardiac troponin T (hs-cTnT) and NH2-terminal pro-brain natriuretic peptide (NT-proBNP). Fifty-eight untrained participants were randomized to supervised endurance exercise (14 wk, 3-4 days/wk, 120-240 min/wk, 65-85% of maximum heart rate) or a control group. At baseline and after the training program, hs-cTnT and NT-proBNP were assessed before and 5 min, 1 h, 3 h, 6 h, 12 h, and 24 h after a 60-min maximal running test. Before training, hs-cTnT was significantly elevated in both groups with acute exercise (P < 0.0001) with no between-group differences. There was considerable heterogeneity in peak hs-cTnT concentration with the upper reference limit exceeded in 71% of the exercise tests. After training, both baseline and postexercise hs-cTnT were significantly higher compared with pretraining and the response of the control group (P = 0.008). Acute exercise led to a small but significant increase in NT-proBNP, but this was not mediated by training (P = 0.121). In summary, a controlled endurance training intervention resulted in higher pre- and postexercise values of hs-cTnT with no changes in NT-proBNP.

Aims The aim of this study was to determine the frequency of heterozygous truncating ALPK3 variants (ALPK3tv) in patients with hypertrophic cardiomyopathy (HCM) and confirm their pathogenicity using burden testing in independent cohorts and family co-segregation studies. Methods and results  In a discovery cohort of 770 index patients with HCM, 12 (1.56%) were heterozygous for ALPK3tv [odds ratio(OR) 16.01, 95% confidence interval (CI) 7.89–29.74, P &lt; 8.36e−11] compared to the Genome Aggregation Database (gnomAD) population. In a validation cohort of 2047 HCM probands, 32 (1.56%) carried heterozygous ALPK3tv (OR 16.17, 95% CI 10.31–24.87, P &lt; 2.2e−16, compared to gnomAD). Combined logarithm of odds score in seven families with ALPK3tv was 2.99. In comparison with a cohort of genotyped patients with HCM (n = 1679) with and without pathogenic sarcomere gene variants (SP+ and SP−), ALPK3tv carriers had a higher prevalence of apical/concentric patterns of hypertrophy (60%, P &lt; 0.001) and of a short PR interval (10%, P = 0.009). Age at diagnosis and maximum left ventricular wall thickness were similar to SP− and left ventricular systolic impairment (6%) and non-sustained ventricular tachycardia (31%) at baseline similar to SP+. After 5.3 ± 5.7 years, 4 (9%) patients with ALPK3tv died of heart failure or had cardiac transplantation (log-rank P = 0.012 vs. SP− and P = 0.425 vs. SP+). Imaging and histopathology showed extensive myocardial fibrosis and myocyte vacuolation. Conclusions  Heterozygous ALPK3tv are pathogenic and segregate with a characteristic HCM phenotype.

We report an unusual case of myopericarditis caused by Rickettsia sibirica mongolitimonae. Because of increasing reports of Rickettsia spp. as etiologic agents of acute myopericarditis and the ease and success with which it was treated in the patient reported here, rickettsial infection should be included in the differential diagnosis for myopericarditis.

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Background The prevalence of cardiac cephalalgia is unknown and there is limited information about its clinical features. We aimed to assess the prevalence of cardiac cephalalgia, its clinical characteristics and associated factors. Methods We conducted a prospective study of patients with suspected acute coronary syndrome admitted to the Cardiology Service at Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain, over a one-year period. We interviewed patients within the first 24 hours of admission using a standardized case-report form to assess the presence of headache in relation to the acute coronary syndrome and its characteristics. Results We included 438 patients, 381 with confirmed myocardial ischemia. Prevalence of cardiac cephalalgia was 14.2% (n = 54). The most common features were frontal location, pressing quality and moderate intensity. Pain referred to the jaws (aOR 2.61; 95% CI 1.33–5.12; p = 0.005), palpitations (aOR 3.65; 95% CI 1.57–8.50; p = 0.003) and circumflex coronary artery as the culprit artery for the myocardial ischemia (aOR 3.8; 95% CI 1.07–13.74; p = 0.021) were related to cardiac whereas history of hypertension was inversely associated (aOR 0.37: 95% CI 0.18–0.74; p = 0.005). Conclusion The prevalence of cardiac cephalalgia was 14.2%. Our study provides valuable information about cardiac cephalalgia characteristics that suggest revision of current diagnostic criteria.