Young athlete's growing heart: sex differences in cardiac adaptation to exercise training during adolescence.

BACKGROUND: Athlete's heart is a condition of exercise-induced cardiac remodelling. Adult male endurance athletes more often remodel beyond reference values. The impact of sex on remodelling through adolescence remains unclear. Paediatric reference values do not account for patient sex or exercise history. We aimed to study the effect of sex on cardiac remodelling throughout adolescence. METHODS: We recruited 76 male (M) and female (F) 12-year-old cross-country skiers in a longitudinal cohort study. Echocardiography was performed and analysed according to guidelines at age 12 (48 M, 28 F), 15 (34 M, 14 F) and 18 (23 M, 11 F). Repeated echocardiographic measurements were analysed by linear mixed model regression. RESULTS: Males displayed greater indexed left ventricular end-diastolic volumes (LV EDVi) from age 12 (M 81±7 vs F 76±7, mL/m², p≤0.01), and progressed further until follow-up at age 18 (M 2.3±9.7 vs F -3.9±4.5 ΔmL/m², p≤0.01). LV EDVi remained above adult upper reference values in both groups. Males increased LV Mass Index from age 12 to 18 (M 33±27 vs F 4±19, Δg/m², p≤0.01). Males displayed LV mass above paediatric reference values at ages 15 and 18. A subset of males (35%) and females (25%) displayed wall thickness above paediatric reference values at age 12. Cardiac function was normal. There was no sex difference in exercise hours. CONCLUSION: Sex-related differences in athlete's heart were evident from age 12, and progressed throughout adolescence. Remodelling beyond reference values was more frequent than previously reported, particularly affecting males. Age, sex and exercise history may assist clinicians in distinguishing exercise-induced remodelling from pathology in adolescents.

Highly malignant disease in childhood-onset arrhythmogenic right ventricular cardiomyopathy.

AIMS: This study aimed to explore the incidence of severe cardiac events in paediatric arrhythmogenic right ventricular cardiomyopathy (ARVC) patients and ARVC penetrance in paediatric relatives. Furthermore, the phenotype in childhood-onset ARVC was described. METHODS: Consecutive ARVC paediatric patients and genotype positive relatives ≤18 years of age were followed with electrocardiographic, structural, and arrhythmic characteristics according to the 2010 revised Task Force Criteria. Penetrance of ARVC disease was defined as fulfilling definite ARVC criteria and severe cardiac events were defined as cardiac death, heart transplantation (HTx) or severe ventricular arrhythmias. Childhood-onset disease was defined as meeting definite ARVC criteria ≤12 years of age. RESULTS: Among 62 individuals [age 9.8 (5.0-14.0) years, 11 probands], 20 (32%) fulfilled definite ARVC diagnosis, of which 8 (40%) had childhood-onset disease. The incidence of severe cardiac events was 23% (n = 14) by last follow-up and half of them occurred in patients ≤12 years of age. Among the eight patients with childhood-onset disease, five had biventricular involvement needing HTx and three had severe arrhythmic events. Among the 51 relatives, 6% (n = 3) met definite ARVC criteria at time of genetic diagnosis, increasing to 18% (n = 9) at end of follow-up. CONCLUSIONS: In a paediatric ARVC cohort, there was a high incidence of severe cardiac events and half of them occurred in children ≤12 years of age. The ARVC penetrance in genotype positive paediatric relatives was 18%. These findings of a high-malignant phenotype in childhood-onset ARVC indicate a need for ARVC family screening at younger age than currently recommended.

Mechanical dispersion as a marker of left ventricular dysfunction and prognosis in stable coronary artery disease.

Assessment of global longitudinal strain (GLS) is superior to ejection fraction (EF) in the evaluation of left ventricular (LV) function in patients with stable coronary artery disease (CAD). However, the role of mechanical dispersion (MD) in this context remains unresolved. We aimed to evaluate the potential role of MD as a marker of LV dysfunction and long-term prognosis in stable CAD. EF, GLS and MD were assessed in 160 patients with stable CAD, 1 year after successful coronary revascularization. Serum levels of high-sensitivity cardiac troponin I (hs-cTnI) and amino-terminal pro B-type natriuretic peptide (NT-proBNP) were quantified as surrogate markers of LV dysfunction. The primary endpoint was defined as all-cause mortality, the secondary endpoint was defined as the composite of all-cause mortality and hospitalization for acute myocardial infarction or heart failure during follow-up. Whereas no associations between EF and the biochemical markers of LV function were found, both GLS and MD correlated positively with increasing levels of hs-cTnI (R = 0.315, P < 0.001 and R = 0.442, P < 0.001, respectively) and NT-proBNP (R = 0.195, P = 0.016 and R = 0.390, P < 0.001, respectively). Median MD was 46 ms (interquartile range [IQR] 37-53) and was successfully quantified in 96% of the patients. During a median follow-up of 8.4 (IQR 8.2-8.8) years, 14 deaths and 29 secondary events occurred. MD was significantly increased in non-survivors, and provided incremental prognostic value when added to EF and GLS. NT-proBNP was superior to the echocardiographic markers in predicting adverse outcomes. MD may be a promising marker of LV dysfunction and adverse prognosis in stable CAD.

Sensitive cardiac troponins and N-terminal pro-B-type natriuretic peptide in stable coronary artery disease: correlation with left ventricular function as assessed by myocardial strain.

N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponins (cTns) measured with sensitive assays provide strong prognostic information in patients with stable coronary artery disease. However, the relationship between these biomarkers and myocardial contractile function, as well as infarct size, in this patient group, remains to be defined. The study population consisted of 160 patients referred to a follow-up echocardiography scheduled 1 year after coronary revascularization. Concentrations of NT-proBNP, high-sensitive cTnT (hs-cTnT) and sensitive cTnI assays were assessed. Left ventricular function was measured as global peak systolic longitudinal strain by speckle tracking echocardiography and infarct size was assessed by late-enhancement MRI. NT-proBNP and sensitive cTnI levels were significantly associated with left ventricular function by peak systolic strain (R-values 0.243 and 0.228, p = 0.002 and 0.004) as well as infarct size (R-values 0.343 and 0.366, p = 0.014 and p = 0.008). In contrast, hs-cTnT did not correlate with left ventricular function (R = 0.095, p = 0.231) and only marginally with infarct size (R = 0.237, p = 0.094). NT-proBNP and sensitive cTnI levels correlate with left ventricular function and infarct size in patients with stable coronary artery disease after revascularization. As opposed to hs-cTnT, NT-proBNP and cTnI seem to be indicators of incipient myocardial dysfunction and the extent of myocardial necrosis.

Mitral annular displacement by Doppler tissue imaging may identify coronary occlusion and predict mortality in patients with non-ST-elevation myocardial infarction.

BACKGROUND: Mitral annular displacement (MAD) is a simple marker of left ventricular (LV) systolic function. The aim of this study was to test the hypothesis that MAD can distinguish patients with non-ST-segment elevation myocardial infarctions (NSTEMIs) from those with significant coronary artery disease without infarctions, identify coronary occlusion, and predict mortality in patients with NSTEMIs. MAD was compared with established indices of LV function. METHODS: In this retrospective study, 167 patients with confirmed NSTEMIs were included at two Scandinavian centers. Forty patients with significant coronary artery disease but without myocardial infarctions were included as controls. Doppler tissue imaging was performed at the mitral level of the left ventricle in the three apical planes, and velocities were integrated over time to acquire MAD. LV ejection fraction, global longitudinal strain (GLS), and wall motion score index were assessed according to guidelines. RESULTS: MAD and GLS could accurately distinguish patients with NSTEMIs from controls. During 48.6 ± 12.1 months of follow-up, 22 of 167 died (13%). MAD, LV ejection fraction, and GLS were reduced and wall motion score index was increased among those who died compared with those who survived (P < .001, P < .001, P < .001, and P = .02, respectively). Multivariate Cox proportional-hazards analyses revealed that MAD was an independent predictor of death (hazard ratio, 1.36; 95% confidence interval, 1.07-1.73; P = .01). MAD and GLS were reduced and wall motion score index was increased in patients with coronary artery occlusion compared with those without occlusion (P = .006, P = .001, and P = .02), while LV ejection fraction did not differ (P = .20). CONCLUSIONS: MAD accurately identified patients with NSTEMIs, predicted mortality, and identified coronary occlusion in patients with NSTEMIs.

Sensitive troponin assays and N-terminal pro-B-type natriuretic peptide in acute coronary syndrome: prediction of significant coronary lesions and long-term prognosis.

BACKGROUND: Sensitive troponin assays have substantially improved early diagnosis of myocardial infarction. However, the role of sensitive cardiac troponin (cTn) assays in prediction of significant coronary lesions and long-term prognosis in non-ST-elevation acute coronary syndrome (NSTE-ACS) remains unresolved. METHODS: This prospective study includes 458 consecutive patients with NSTE-ACS admitted for coronary angiography. Serum levels of 4 commercial available sensitive troponin assays were analyzed (Roche high-sensitive cTnT [hs-cTnT; Roche Diagnostics, Basel, Switzerland], Siemens cTnI Ultra [Siemens, Munich, Germany], Abbott-Architect cTnI [Abbott, Abbott Park, IL], Access Accu-cTnI [Beckman Coulter, Nyon, Switzerland]), as well as a standard assay (Roche cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), before coronary angiography. RESULTS: The relationship between the analyzed biomarkers and significant coronary lesions on coronary angiography, as quantified by area under the receiver operating characteristic curve, was significantly higher with Roche hs-cTnT, Siemens cTnI Ultra, and Access Accu-cTnI as compared with standard troponin T assay (P < .001 for all comparisons). This difference was mainly caused by increased sensitivity below the 99th percentile. Also, NT-proBNP was associated with the presence of significant coronary lesions. Cardiac troponin values were correlated with cardiac death (primary end point) during 1373 (1257-1478) days of follow-up. In both univariate and multivariate Cox regression analyses, NT-proBNP was superior to both hs-cTnT and cTnI in prediction of cardiovascular mortality. Troponin values with all assays were correlated with the need for repeated revascularization (secondary end point) during follow-up. CONCLUSIONS: Sensitive cTn assays are superior to standard cTnT assay in prediction of significant coronary lesions in patients with NSTE-ACS. However, this improvement is primary caused by increased sensitivity below the 99th percentile. N-terminal pro-B-type natriuretic peptide is superior to cTns in prediction of long-term mortality.

Duration of myocardial early systolic lengthening predicts the presence of significant coronary artery disease.

OBJECTIVES: This study sought to investigate whether the duration of left ventricular (LV) early systolic lengthening could accurately identify patients with significant coronary artery disease (CAD). BACKGROUND: Ischemic myocardium with reduced active force will lengthen when LV pressure rises during early systole before onset of systolic shortening. METHODS: We included 88 patients with suspected CAD referred to elective diagnostic coronary angiography. Two of these patients were excluded from the study due to evidence of previous myocardial infarction on contrast-enhanced magnetic resonance imaging. Speckle tracking echocardiography was performed before coronary angiography and at follow-up scheduled 1 year after revascularization, and global longitudinal strain and duration of average LV early systolic lengthening were recorded. RESULTS: Forty-three of 86 patients had significant CAD. The duration of early systolic lengthening was significantly prolonged in patients with significant CAD compared with patients without significant coronary artery stenoses (76 ± 37 ms vs. 38 ± 23 ms, p < 0.001). Correspondingly, global systolic strain was significantly lower in patients with CAD (-17.7 ± 3.0% vs. -19.5 ± 2.6%, p = 0.003). Prolonged duration of early systolic lengthening showed the best accuracy in detecting CAD, with an area under the receiver-operating characteristic curve of 0.83. The area under the curve for global strain was 0.68. At 1-year follow-up, the duration of early systolic lengthening was significantly reduced (64 ± 37 ms vs. 76 ± 37 ms, p = 0.041) in the patients treated with revascularization. CONCLUSIONS: Duration of myocardial early systolic lengthening was prolonged in patients with significant CAD; this might be a useful parameter to identify patients who might benefit from reperfusion therapy.

Detection of left ventricular dysfunction by global longitudinal systolic strain in patients with chronic aortic regurgitation.

BACKGROUND: The purpose of this study was to investigate whether global longitudinal strain measured by two-dimensional speckle tracking echocardiography could detect incipient myocardial dysfunction in patients with chronic aortic regurgitation (AR). Disclosing left ventricular (LV) dysfunction is of decisive importance for optimal timing of surgery but challenging because of the altered loading conditions. METHODS: Forty-seven patients referred for aortic valve replacement because of chronic AR were studied, along with 31 healthy controls. Myocardial deformation as determined by longitudinal, circumferential, and radial strain was calculated using two-dimensional speckle-tracking echocardiography technique, in addition to LV volumes, dimensions, and ejection fraction. Strain values were normalized to end-diastolic volume to correct for the volume dependency of deformation. RESULTS: Global systolic longitudinal strain was significantly lower in patients with AR before surgery compared with the healthy controls (-17.5 ± 3.1% vs -22.1 ± 1.8%, P < .01), while global circumferential strain and LV ejection fraction did not differ (-21.7 ± 3.4% vs -22.6 ± 2.5%, P = .22 and 59 ± 5% vs 59 ± 6%, P = .59, respectively). However, differences between patients and controls were evident for both longitudinal and circumferential strain when normalized to end-diastolic volume (-0.09 ± 0.04 vs -0.23 ± 0.08, P < .01, and -0.11 ± 0.05 vs -0.24 ± 0.08, P < .01, respectively). In contrast to their absolute values, both normalized variables demonstrated improvement in myocardial shortening after valve replacement (P < .01). CONCLUSIONS: The study demonstrated reduced global longitudinal strain in patients with chronic AR with preserved LV ejection fractions. Global longitudinal strain might therefore disclose incipient myocardial dysfunction with a consequent potential for improved timing of aortic valve surgery.

Mechanical dispersion assessed by myocardial strain in patients after myocardial infarction for risk prediction of ventricular arrhythmia.

OBJECTIVES: The aim of this study was to investigate whether myocardial strain echocardiography can predict ventricular arrhythmias in patients after myocardial infarction (MI). BACKGROUND: Left ventricular (LV) ejection fraction (EF) is insufficient for selecting patients for implantable cardioverter-defibrillator (ICD) therapy after MI. Electrical dispersion in infarcted myocardium facilitates malignant arrhythmia. Myocardial strain by echocardiography can quantify detailed regional and global myocardial function and timing. We hypothesized that electrical abnormalities in patients after MI will lead to LV mechanical dispersion, which can be measured as regional heterogeneity of contraction by myocardial strain. METHODS: We prospectively included 85 post-MI patients, 44 meeting primary and 41 meeting secondary ICD prevention criteria. After 2.3 years (range 0.6 to 5.5 years) of follow-up, 47 patients had no and 38 patients had 1 or more recorded arrhythmias requiring appropriate ICD therapy. Longitudinal strain was measured by speckle tracking echocardiography. The SD of time to maximum myocardial shortening in a 16-segment LV model was calculated as a parameter of mechanical dispersion. Global strain was calculated as average strain in a 16-segment LV model. RESULTS: The EF did not differ between ICD patients with and without arrhythmias occurring during follow-up (34 +/- 11% vs. 35 +/- 9%, p = 0.70). Mechanical dispersion was greater in ICD patients with recorded ventricular arrhythmias compared with those without (85 +/- 29 ms vs. 56 +/- 13 ms, p < 0.001). By Cox regression, mechanical dispersion was a strong and independent predictor of arrhythmias requiring ICD therapy (hazard ratio: 1.25 per 10-ms increase, 95% confidence interval: 1.1 to 1.4, p < 0.001). In patients with an EF >35%, global strain showed better LV function in those without recorded arrhythmias (-14.0% +/- 4.0% vs. -12.0 +/- 3.0%, p = 0.05), whereas the EF did not differ (44 +/- 8% vs. 41 +/- 5%, p = 0.23). CONCLUSIONS: Mechanical dispersion was more pronounced in post-MI patients with recurrent arrhythmias. Global strain was a marker of arrhythmias in post-MI patients with relatively preserved ventricular function. These novel parameters assessed by myocardial strain may add important information about susceptibility for ventricular arrhythmias after MI.

[Psychological intervention after trauma--does it work?]. / Psykologisk intervensjon etter traumer - gjør det vondt verre?

A Cochrane review from 1998 concluded that single-session intervention does not prevent the onset of post-traumatic stress disorder. This led to a debate about what is the best, if any, psychological treatment after traumas. In consequence, some clinicians have become doubtful about as how to deal with traumatized patients. We present three examples in order to illustrate situations in which psychological intervention is useful. The conclusions in the Cochrane review are well documented. However, insufficient correspondence between the traumas and the intervention offered gave us cause to question the clinical importance of existing studies. Future studies of psychological intervention after traumas should use an individualized design in which the intervention is in proportion to the trauma. Based on knowledge not given by randomized controlled studies, we recommend clinicians to offer psychological help to those exposed to traumatic incidents. Most people need adequate information after traumas. For those who develop health problems, intervention until recovery is recommended.