The relationship between workload and exercise-induced cardiac troponin elevations is influenced by non-obstructive coronary atherosclerosis.

The relationship between exercise-induced troponin elevation and non-obstructive coronary artery disease (CAD) is unclear. This observational study assessed non-obstructive CAD's impact on exercise-induced cardiac Troponin I (cTnI) elevation in middle-aged recreational athletes. cTnI levels of 40 well-trained recreational athletes (73% males, 50 ± 9 years old) were assessed by a high-sensitive cTnI assay 24 h before, and at 3 and 24 h following two high-intensity exercises of different durations; a cardiopulmonary exercise test (CPET), and a 91-km mountain bike race. Workload was measured with power meters. Coronary computed tomography angiography was used to determine the presence or absence of non-obstructive (<50% obstruction) CAD. A total of 15 individuals had non-obstructive CAD (Atherosclerotic group), whereas 25 had no atherosclerosis (normal). There were higher post-exercise cTnI levels following the race compared with CPET, both at 3 h (77.0 (35.3-112.4) ng/L vs. 11.6 (6.4-22.5) ng/L, p < 0.001) and at 24 h (14.7 (6.7-16.3) vs. 5.0 (2.6-8.9) ng/L, p < 0.001). Absolute cTnI values did not differ among groups. Still, the association of cTnI response to power output was significantly stronger in the CAD versus Normal group both at 3 h post-exercise (Rho = 0.80, p < 0.001 vs. Rho = -0.20, p = 0.33) and 24-h post-exercise (Rho = 0.87, p < 0.001 vs. Rho = -0.13, p = 0.55). Exercise-induced cTnI elevation was strongly correlated with exercise workload in middle-aged athletes with non-obstructive CAD but not in individuals without CAD. This finding suggests that CAD influences the relationship between exercise workload and the cTnI response even without coronary artery obstruction.

Exercise-Induced Cardiac Troponin Elevations: From Underlying Mechanisms to Clinical Relevance.

Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field.

Circulating trimethylamine N-oxide levels do not predict 10-year survival in patients with or without coronary heart disease.

BACKGROUND: Trimethylamine N-oxide (TMAO) is an amine oxide generated by gut microbial metabolism. TMAO may contribute to atherothrombosis and systemic inflammation. However, the prognostic value of circulating TMAO for risk stratification is uncertain. METHODS: We assessed prospective relationships of plasma TMAO with long-term risk of all-cause, cardiovascular (CV), and non-CV mortality in the Western Norway Coronary Angiography Cohort (WECAC; 4132 patients with suspected coronary artery disease) and the Hordaland Health Study (HUSK; 6393 community-based subjects). Risk associations were examined using Cox regression analyses. RESULTS: Mean follow-up was 9.8 and 10.5 years in WECAC and HUSK, respectively. Following adjustments for established CV risk factors and indices of renal function in WECAC, the hazard ratios (HRs) (95% confidence intervals [CIs]) per one standard deviation increase in log-transformed plasma TMAO were 1.04 (0.97-1.12), 1.06 (0.95-1.18), and 1.03 (0.93-1.13) for all-cause, CV, and non-CV mortality, respectively. Essentially similar results were obtained in patients with angiographically significant coronary artery disease and patients with reduced left ventricular ejection fraction. Corresponding HRs (95% CIs) in the HUSK cohort were 1.03 (0.96-1.10), 1.01 (0.89-1.13), and 1.03 (0.95-1.12) for all-cause-, CV, and non-CV mortality, respectively. CONCLUSIONS: Circulating TMAO did not predict long-term all-cause, CV, or non-CV mortality in patients with coronary heart disease or in community-based adults. This large study does not support a role of TMAO for patient risk stratification in primary or secondary prevention.

Endurance exercise training volume is not associated with progression of coronary artery calcification.

BACKGROUND: Recent cross-sectional studies have suggested a dose-dependent relationship between lifelong exposure to physical activity and the burden of calcified coronary artery disease (CAD). No longitudinal studies have addressed this concern. HYPOTHESIS: Exercise volume is associated with progression of coronary artery calcium (CAC), defined as ≥10 units increase in CAC score. METHODS: Sixty-one recreational athletes who were assessed by coronary computed tomography angiography (CCTA) as part of the NEEDED 2013/14 study were re-assessed 4-5 years later, in 2018. RESULTS: Subjects were 45.9 ± 9.6 years old at inclusion, and 46 (74%) were male. Between 2013 and 2018, the participants reported median 5 (range: 0-20, 25th-75th percentile: 4-6) hours of high-intensity exercise per week. None of the included subjects smoked during follow-up. At inclusion, 21 (33%) participants had coronary artery calcifications. On follow-up CCTA in 2018, 15 (25%) subjects had progressive coronary calcification (≥10 Agatston units increase in CAC). These subjects were older (53 ± 9 vs 44 ± 9 years old, P = .002) and had higher levels of low-density lipoprotein at baseline (3.5 (2.9-4.3) vs 2.9 (2.3-3.5) mmol/L, P = .031) as compared to subjects with stable condition. No relationship was found between hours of endurance training per week and progression of coronary artery calcification. In multiple regression analysis, age and baseline CAC were the only significant predictors of progressive CAC. CONCLUSION: No relationship between exercise training volume and the progression of coronary artery calcification was found in this longitudinal study of middle-aged recreational athletes.

Artifact Correction in Short-Term HRV during Strenuous Physical Exercise.

Heart rate variability (HRV) analysis can be a useful tool to detect underlying heart or even general health problems. Currently, such analysis is usually performed in controlled or semi-controlled conditions. Since many of the typical HRV measures are sensitive to data quality, manual artifact correction is common in literature, both as an exclusive method or in addition to various filters. With proliferation of Personal Monitoring Devices with continuous HRV analysis an opportunity opens for HRV analysis in a new setting. However, current artifact correction approaches have several limitations that hamper the analysis of real-life HRV data. To address this issue we propose an algorithm for automated artifact correction that has a minimal impact on HRV measures, but can handle more artifacts than existing solutions. We verify this algorithm based on two datasets. One collected during a recreational bicycle race and another one in a laboratory, both using a PMD in form of a GPS watch. Data include direct measurement of electrical myocardial signals using chest straps and direct measurements of power using a crank sensor (in case of race dataset), both paired with the watch. Early results suggest that the algorithm can correct more artifacts than existing solutions without a need for manual support or parameter tuning. At the same time, the error introduced to HRV measures for peak correction and shorter gaps is similar to the best existing solution (Kubios-inspired threshold-based cubic interpolation) and better than commonly used median filter. For longer gaps, cubic interpolation can in some cases result in lower error in HRV measures, but the shape of the curve it generates matches ground truth worse than our algorithm. It might suggest that further development of the proposed algorithm may also improve these results.

[Cardiac sarcoidosis]. / Kardial sarkoidose.

Sarcoidosis is characterised by granulomatous inflammation in one or more organs, including the heart. Cardiac sarcoidosis generally has non-specific symptoms, and the disease is often diagnosed at a late stage. The condition is associated with cardiomyopathy and arrhythmia and may be fatal.

Circulating Galectin-3 Levels Are Increased in Patients with Ischemic Heart Disease, but Are Not Influenced by Acute Myocardial Infarction.

OBJECTIVES: Galectin-3 (Gal-3) is involved in cardiac inflammation and fibrosis, and is in use as a biomarker that indicates increased risk in heart failure. This study examined the relationship between Gal-3 levels and acute and old myocardial infarction (MI) in patients assessed by cardiac magnetic resonance (CMR) imaging. METHODS: Group 1 consisted of 38 patients with ST-elevation MI and single-vessel disease treated with primary percutaneous coronary intervention (PCI). Group 2 consisted of 52 patients with prior complicated MI. Twenty-two controls were included. CMR was performed in group 1 at 2 days, 1 week, 2 months and 1 year following PCI and in group 2 at >4 years after MI. RESULTS: Median Gal-3 was elevated in patients compared with controls, group 1: 11.93 ng/ml (IQR 6.34-17.52, p = 0.03), group 2: 12.96 (IQR 6.33-19.29, p = 0.03) and controls: 10.16 (IQR 5.59-14.73). Gal-3 levels did not change during acute MI, and there was no relationship between Gal-3 and infarct size, troponin-T, high-sensitivity C-reactive protein, left-ventricular (LV) volumes or LV ejection fraction (LVEF) in group 1. In group 2, Gal-3 correlated modestly with MI size (r = 0.28, p < 0.05), LV end-diastolic volume index (r = 0.40, p < 0.01), LV end-systolic volume index (r = 0.43, p < 0.01) and LVEF (r = -0.39, p < 0.01). CONCLUSION: There was no relationship between Gal-3 levels and acute ischemic myocardial injury. A significant, modest relationship between Gal-3 levels, MI size and LV remodeling was only found in patients with old MI.

The relationship between transmurality of ischemic scars and the heart rate of ventricular tachycardia.

AIMS: The relationship between the heart rate of ventricular tachycardia (VT) and the transmurality of ischemic scars was assessed by a new semiautomatic coordinate-based analysis of late gadolinium-enhanced cardiac magnetic resonance (LGE-CMR) images. METHODS AND RESULTS: Twenty patients assessed by LGE-CMR before implantation of implantable cardioverter defibrillator (ICD) with verified VT during the first year following ICD implantation were included. Scar was defined by pixels with a signal intensity ≥ 50% of maximum signal intensity. All pixels were assigned a coordinate position between endo- and epicardium (λ) and the angle of the heart axis (φ). Based upon the λ and φ values, multiple scar features were computed for all scarred areas. These features were correlated to VT heart rate across the complete range of transmurality. The strongest correlation with univariate regression was found between VT heart rate and the sum of transmurality when the maximum transmurality of these features was ≥ 90% (R-square = 0.47). In multiple regressions analysis, the strongest relationship with VT heart rate was found with a maximum transmurality ≥ 90% and by a combination of scar size, transmurality, and endocardial extent of infarction (R-square = 0.64). CONCLUSION: Transmurality is the strongest predictor of VT heart rate both in univariate and multivariate models. The strongest relationships were found at a transmurality level > 90%.

The relationship between markers of extracellular cardiac matrix turnover: infarct healing and left ventricular remodelling following primary PCI in patients with first-time STEMI.

AIMS: We investigated the temporal changes in circulating levels of markers of extracellular cardiac matrix (ECCM) turnover and their relationship with infarct size (IS), ejection fraction (EF), and left ventricular (LV) volumes, determined by serial cardiac magnetic resonance (CMR) imaging in patients with first-time ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS: Forty-two patients with a first-time STEMI, successfully revascularized by primary percutaneous coronary intervention (pPCI) had serum samples taken prior to pPCI, 2, 7 days, 2 months, and 1 year following STEMI for the analysis of the markers of collagen synthesis, and collagen degradation. Late enhancement and cine CMR was performed on Days 2, 7, 2 months, and 1-year post-STEMI. There was a significant increase in type I collagen degradation following STEMI that was not accompanied by an increase in collagen type I synthesis until 2 months and 1 year. In contrast to the delay in type I collagen synthesis, there was an immediate increase in type III collagen synthesis that was sustained for 1 year. N-terminal procollagen type I levels assessed prior to pPCI were predictive of adverse LV remodelling at all CMR time-points. CONCLUSIONS: Our findings indicate a net type I collagen breakdown in the first week following STEMI compensated by an early increase in collagen type III synthesis. There is an increase in both type I and III collagen synthesis markers at 2 months and 1 year, indicating a persistent increase in collagen turnover even in these apparently successfully treated patients.

Changes in 6-min walk test is an independent predictor of death in chronic heart failure with reduced ejection fraction.

AIMS: Functional capacity provides important clinical information in patients with heart failure (HF) and reduced ejection fraction (HFrEF). The 6-min walk test (6MWT) is a simple and inexpensive tool for assessing functional capacity and risk. Although change in 6MWT is frequently used as a surrogate outcome in HF trials, the association with mortality is unclear. We aimed to assess the prognostic importance of changes in 6MWT. METHODS AND RESULTS: Patients with chronic HFrEF referred to HF outpatient clinics in Norway completed a 6MWT at the first visit (baseline) and at a stable follow-up visit after treatment optimization (follow-up). Absolute and relative changes in 6MWT were analysed in association with mortality risk using Cox regression models and flexible cubic splines. The study included 3636 HFrEF patients aged 67.3 ± 11.6 years, 23% women, with left ventricular ejection fraction 30 ± 7%. At baseline, mean 6MWT was 438 ± 125 m, median N-terminal pro-B-type natriuretic peptide (NT-proBNP) 1574 (732-3093) ng/L, and 27% had New York Heart Association (NYHA) class III/IV. After optimization of guideline-directed medical therapy (median 147 [86-240] days), 6MWT increased by mean 40 ± 74 m, NT-proBNP decreased by median 425 (14-1322) ng/L, and NYHA class improved in 38% of patients. Patients with greater improvements in 6MWT were younger, with greater improvements in NYHA class (r = 0.27, p < 0.001) and larger reductions in NT-proBNP concentrations (r = 0.19, p < 0.001). After mean 845 ± 595 days, 419 (11.5%) patients were dead. Both absolute and relative changes in 6MWT were non-linearly associated with survival, attenuating as 6MWT increased. A 50 m increase in 6MWT was associated with a 17% lower mortality risk (hazard ratio 0.84, 95% confidence interval 0.77-0.90, p < 0.001) in the fully adjusted model, including changes in NYHA class, NT-proBNP concentrations, and other established risk factors. The associations were more pronounced in patients with lower baseline 6MWT and higher age. CONCLUSION: Improvement in 6MWT in patients with HFrEF is associated with increased survival, independent of changes in NT-proBNP and NYHA class. These findings support 6MWT change as a surrogate outcome in HF trials.

High dose statin treatment reduces circulating Dickkopf-1 following acute myocardial infarction.

BACKGROUND: Secreted glycoproteins of the Dickkopf (DKK) family modify Wnt signaling and may influence plaque destabilization but their modulation by statins in MI patients is not known. METHODS: We measured plasma DKK-1 and DKK-3 in patients with acute ST-segment elevation MI (STEMI) before percutaneous coronary intervention (PCI) and after 2 and 7 days and 2 months in patients receiving short-term high-dose (40 mg rosuvastatin, given before PCI; n = 25) and moderate dose (20 mg simvastatin, given the day after PCI; n = 34). In vitro modulation of DKK-1 in human umbilical vein endothelial cells (HUVECs) by statins were assessed. RESULTS: (i) Patients receiving high dose rosuvastatin had a marked decline in DKK-1 at day 2 which was maintained throughout the study period. However, a more prevalent use of ß-blockers in the simvastatin group, that could have contributed to higher DKK-1 levels in these patients. (ii) There was a strong correlation between baseline DKK-1 levels and change in DKK-1 from baseline to day 2 in patients receiving high dose rosuvastatin treatment. (iii) DKK-3 increased at day 2 but returned to baseline levels at 2 months in both treatment groups. (iv) Statin treatment dose-dependently decreased DKK-1 mRNA and protein levels in HUVEC. CONCLUSIONS: Our findings suggest that high dose statin treatment with 40 mg rosuvastatin could persistently down-regulate DKK-1 levels, even at 2 months after the initial event in STEMI patients.

Probability mapping of scarred myocardium using texture and intensity features in CMR images.

BACKGROUND: The myocardium exhibits heterogeneous nature due to scarring after Myocardial Infarction (MI). In Cardiac Magnetic Resonance (CMR) imaging, Late Gadolinium (LG) contrast agent enhances the intensity of scarred area in the myocardium. METHODS: In this paper, we propose a probability mapping technique using Texture and Intensity features to describe heterogeneous nature of the scarred myocardium in Cardiac Magnetic Resonance (CMR) images after Myocardial Infarction (MI). Scarred tissue and non-scarred tissue are represented with high and low probabilities, respectively. Intermediate values possibly indicate areas where the scarred and healthy tissues are interwoven. The probability map of scarred myocardium is calculated by using a probability function based on Bayes rule. Any set of features can be used in the probability function. RESULTS: In the present study, we demonstrate the use of two different types of features. One is based on the mean intensity of pixel and the other on underlying texture information of the scarred and non-scarred myocardium. Examples of probability maps computed using the mean intensity of pixel and the underlying texture information are presented. We hypothesize that the probability mapping of myocardium offers alternate visualization, possibly showing the details with physiological significance difficult to detect visually in the original CMR image. CONCLUSION: The probability mapping obtained from the two features provides a way to define different cardiac segments which offer a way to identify areas in the myocardium of diagnostic importance (like core and border areas in scarred myocardium).

Optimizing support vector machines and autoregressive integrated moving average methods for heart rate variability data correction.

Heart rate variability (HRV) is the variation in time between successive heartbeats and can be used as an indirect measure of autonomic nervous system (ANS) activity. During physical exercise, movement of the measuring device can cause artifacts in the HRV data, severely affecting the analysis of the HRV data. Current methods used for data artifact correction perform insufficiently when HRV is measured during exercise. In this paper we propose the use of autoregressive integrated moving average (ARIMA) and support vector regression (SVR) for HRV data artifact correction. Since both methods are only trained on previous data points, they can be applied not only for correction (i.e., gap filling), but also prediction (i.e., forecasting future values). Our paper describes:•why HRV is difficult to predict and why ARIMA and SVR might be valuable options.•finding the best hyperparameters for using ARIMA and SVR to correct HRV data, including which criterion to use for choosing the best model.•which correction method should be used given the data at hand.

The Association of Smoking with Hospitalization and Mortality Differs According to Sex in Patients with Heart Failure Following Myocardial Infarction.

Background: Smoking has been associated with higher morbidity and mortality following myocardial infarction (MI), but reports of the impact on morbidity and mortality for females and elderly patients experiencing MI complicated with left ventricular dysfunction or overt heart failure are limited. Materials and Methods: In an individual patient data meta-analysis of high-risk MI patients, the association of smoking with hospitalizations and death were investigated. Weighted Cox proportional hazard modeling were used to study the risks of smoking on adjudicated endpoints among different sex and age categories. Results: Twenty-eight thousand seven hundred thirty-five patients from the CAPRICORN, EPHESUS, OPTIMAAL, and VALIANT trials were assessed. After weighting, smokers (N = 18,148) were unfrequently women (29.2%) and a minority were above ≥80 years (9.8%). Smoking was significantly more associated with all-cause hospitalizations in women (hazard ratio [HR] 1.24; 95% confidence interval [95% CI] 1.16-1.32) than in men (HR = 1.10; 95% CI 1.05-1.16) resulting in a significant interaction between smoking and sex (p = 0.005). Smoking was predictive of all-cause mortality homogenously across age categories (p for interaction = 0.25) and sex (p for interaction = 0.58). Conclusions: The influence of smoking on morbidity differed according to sex following high-risk MI. The deleterious impact of smoking on hospitalization appeared particularly potent in women, which should further reinforce preventive strategies in females.

Cardiac Structure and Function in Epilepsy Patients with Drug-Resistant Convulsive Seizures.

High frequency of convulsive seizures and long-lasting epilepsy are associated with an increased risk of sudden unexpected death in epilepsy (SUDEP). Structural changes in the myocardium have been described in SUDEP victims. It is speculated that these changes are secondary to frequent convulsive seizures and may predispose to SUDEP. The aim of this cross-sectional study was to investigate the impact of chronic drug-resistant epilepsy on cardiac function and structure in patients with a high frequency of convulsive seizures. We consecutively included 21 patients (17 women, 4 men) aged 18-40 years, with at least 10 years with epilepsy and a minimum of six convulsive seizures in the last year and without a history of status epilepticus or nonepileptic events. A complete clinical examination, resting 12-lead electrocardiogram, 72-h Holter monitoring, and echocardiography were recorded in all patients. Ten patients were assessed by 3-Tesla cardiac magnetic resonance imaging. Echocardiography and MRI data were compared with those from age- and sex-matched healthy control individuals. No significant changes in cardiac structure or function were found among patients with chronic drug-resistant epilepsy and high frequency of convulsive seizures. However, we cannot exclude that there are subgroups of patients who are more prone to epilepsy-associated cardiac alterations.

Myocardial inefficiency is an early indicator of exercise-induced myocardial fatigue.

Background: The effect of prolonged, high-intensity endurance exercise on myocardial function is unclear. This study aimed to determine the left ventricular (LV) response to increased exercise duration and intensity using novel echocardiographic tools to assess myocardial work and fatigue. Materials and methods: LV function was assessed by echocardiography before, immediately, and 24 h after a cardiopulmonary exercise test (CPET) and a 91-km mountain bike leisure race. Cardiac Troponin I (cTnI) was used to assess myocyte stress. Results: 59 healthy recreational athletes, 52 (43-59) years of age, 73% males, were included. The race was longer and of higher intensity generating higher cTnI levels compared with the CPET (p < 0.0001): Race/CPET: exercise duration: 230 (210, 245)/43 (40, 45) minutes, mean heart rate: 154 ± 10/132 ± 12 bpm, max cTnI: 77 (37, 128)/12 (7, 23) ng/L. Stroke volume and cardiac output were higher after the race than CPET (p < 0.005). The two exercises did not differ in post-exercise changes in LV ejection fraction (LVEF) or global longitudinal strain (GLS). There was an increase in global wasted work (p = 0.001) following the race and a persistent reduction in global constructive work 24 h after exercise (p = 0.003). Conclusion: Increased exercise intensity and duration were associated with increased myocardial wasted work post-exercise, without alterations in LVEF and GLS from baseline values. These findings suggest that markers of myocardial inefficiency may precede reduction in global LV function as markers of myocardial fatigue.

The heart rate of ventricular tachycardia following an old myocardial infarction is inversely related to the size of scarring.

AIMS: The purpose of the study was to examine the relationship between the initial cycle length (CL) of ventricular tachycardia (VT) and the size of the myocardial scar and its border zone in patients with old myocardial infarction (MI). METHODS AND RESULTS: Late gadolinium-enhancement cardiac magnetic resonance was performed prior to implantable cardioverter-defibrillator (ICD) implantation in 24 patients. The size of non-scared myocardium, scar, scar core, and border zone were measured as voxel numbers. The number of core islands, contour-regularity of scar and left-ventricular ejection fraction were also calculated. During the first year after ICD implantation, VT was recorded in 20 patients. With univariate regression analysis, the number of core islands had the highest correlation with the CL of VT (R = 0.614, adjusted R(2) = 0.342, P = 0.004). By multiple regression analyses, the highest correlation was found by the use of scar core and core islands (R = 0.721, adjusted R(2) = 0.464, P = 0.002). CONCLUSION: The heart rate of VT (bpm) in patients with old MI is inversely related to the properties of the densest parts of the myocardial scar.

Texture-based probability mapping for automatic scar assessment in late gadolinium-enhanced cardiovascular magnetic resonance images.

PURPOSE: To evaluate a novel texture-based probability mapping (TPM) method for scar size estimation in LGE-CMRI. METHODS: This retrospective proof-of-concept study included chronic myocardial scars from 52 patients. The TPM was compared with three signal intensity-based methods: manual segmentation, full-width-half-maximum (FWHM), and 5-standard deviation (5-SD). TPM is generated using machine learning techniques, expressing the probability of scarring in pixels. The probability is derived by comparing the texture of the 3 × 3 pixel matrix surrounding each pixel with reference dictionaries from patients with established myocardial scars. The Sørensen-Dice coefficient was used to find the optimal TPM range. A non-parametric test was used to test the correlation between infarct size and remodeling parameters. Bland-Altman plots were performed to assess agreement among the methods. RESULTS: The study included 52 patients (76.9% male; median age 64.5 years (54, 72.5)). A TPM range of 0.328-1.0 was found to be the optimal probability interval to predict scar size compared to manual segmentation, median dice (25th and 75th percentiles)): 0.69(0.42-0.81). There was no significant difference in the scar size between TPM and 5-SD. However, both 5-SD and TPM yielded larger scar sizes compared with FWHM (p < 0.001 and p = 0.002). There were strong correlations between scar size measured by TPM, and left ventricular ejection fraction (LVEF, r = -0.76, p < 0.001), left ventricular end-diastolic volume index (r = 0.73, p < 0.001), and left ventricular end-systolic volume index (r = 0.75, p < 0.001). CONCLUSION: The TPM method is comparable with current SI-based methods, both for the scar size assessment and the relationship with left ventricular remodeling when applied on LGE-CMRI.

Regular consumption of cod liver oil is associated with reduced basal and exercise-induced C-reactive protein levels; a prospective observational trial : A NEEDED (The North Sea Race Endurance Exercise Study) 2014 sub-study.

BACKGROUND: Dietary supplement use among recreational athletes is common, with the intention of reducing inflammation and improving recovery. We aimed to describe the relationship between omega-3 fatty acid supplement use and inflammation induced by strenuous exercise. METHODS: C-reactive protein (CRP) concentrations were measured in 1002 healthy recreational athletes before and 24 h after a 91-km bicycle race. The use of omega-3 fatty acid supplements was reported in 856 out of 1002 recreational athletes, and the association between supplement use and the exercise-induced CRP response was assessed. RESULTS: Two hundred seventy-four subjects reported regular use of omega-3 fatty acid supplements. One hundred seventy-three of these used cod liver oil (CLO). Regular users of omega-3 fatty acid supplements had significantly lower basal and exercise-induced CRP levels as compared to non-users (n = 348, p < 0.001). Compared to non-users, regular users had a 27% (95% confidence interval (CI): 14-40) reduction in Ln CRP response (unadjusted model, p < 0.001) and 16% (95% CI: 5-28, p = 0.006) reduction after adjusting for age, sex, race duration, body mass index, delta creatine kinase, MET hours per week, resting heart rate and higher education. CLO was the primary driver of this response with a 34% (95% CI: 19-49) reduction (unadjusted model, p < 0.001) compared to non-users. Corresponding numbers in the adjusted model were 24% (95% CI: 11-38, p < 0.001). CONCLUSION: Basal CRP levels were reduced, and the exercise-induced CRP response was attenuated in healthy recreational cyclists who used omega-3 fatty acid supplements regularly. This effect was only present in regular users of CLO. TRIAL REGISTRATION: NCT02166216 , registered June 18, 2014 - Retrospectively registered.