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.
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.
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.
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.
Studies of patients with acute myocardial infarction (MI) suggest that anterior transmural infarcts are associated with greater left ventricular (LV) remodeling compared with nontransmural ...nonanterior infarctions. It is unclear whether this relation also exists in long-term survivors of MI. Cardiac magnetic resonance imaging was used to explore the relation between myocardial scar size, localization, transmurality, and degree of long-term LV remodeling in patients with healed MI. Subjects were recruited from a registry of patients with healed MI who participated in the OPTIMAAL trial. Cardiac magnetic resonance imaging was performed to assess LV mass, volumes, LV ejection fraction, and myocardial scarring, adjusting for myocardial ischemia. Fifty-seven patients (mean age 69 ± 10 years mean ejection fraction 49 ± 13%) were studied 4.4 ± 0.4 years after MI. Anterior scar was found in 19 patients and nonanterior scar in 33, whereas 5 patients did not show myocardial scar. Transmural scar was evident in 36 patients. In the 52 patients with scar, average total scar size was 13 ± 8% of total LV mass. There was a strong linear relation between scar size and LV end-diastolic volume index (r = 0.81, p <0.0001), end-systolic volume index (r = 0.86, p <0.0001), and LV ejection fraction (r = −0.74, p <0.0001). In multivariate analysis, scar size was the strongest independent predictor of ejection fraction and LV volumes independently of scar localization and transmurality. In conclusion, in the studied cohort, there was a linear relation between scar size and ejection fraction and LV volumes. This relation was independent of scar location and transmurality.
Aims We studied the time-dependent relationships between microvascular obstruction (MO), infarct size, and left ventricular (LV) remodelling after acute myocardial infarction (MI). Methods and ...results Forty-two consecutive patients with first-time ST-elevation MI, single-vessel disease, successfully treated with primary percutaneous coronary intervention (PCI) were included. Microvascular obstruction, infarct size, and LV remodelling were assessed by cardiac magnetic resonance. Cardiac magnetic resonance was performed at: 2 days, 1 week, 2 months, and 1 year following PCI. Microvascular obstruction was assessed by first-pass perfusion. Patients were divided into three groups according to the presence or absence of MO at 2 days and 1 week: no detectable MO at any time point (11 patients), MO detectable only at 2 days (16 patients), and MO detectable both at 2 days and 1 week (15 patients). In multivariable analysis adjusting for infarct size at 2 days, detectable MO at 1 week was an independent predictor (P = 0.003) of infarct size at 1 year follow-up, associated with adverse infarct healing, adverse LV remodelling, increased LV volumes, and lower ejection fractions when compared with the rest of the cohort. Conclusion Microvascular obstruction is an important determinant of infarct healing. The effect of MO on infarct size translated into distinct patterns of LV remodelling during long-term follow-up. Clinical study no.: NCT 00465868
Aims This study assessed the relationship between inflammatory mediators and indices of infarct size and left-ventricular (LV) remodelling following successful primary percutaneous coronary ...intervention (PCI) in patients with first time ST elevation myocardial infarction (MI). Methods and results Forty-two patients admitted with an occluded single vessel were recruited consecutively. Cardiac magnetic resonance was used for serial assessment (2 days, 1 week, 2 months) of infarct size, microvascular obstruction (MO), and LV remodelling. Inflammatory mediators were analysed before and after PCI. Our major findings were: (1) Following PCI, there was a marked increase in plasma levels of C-reactive protein, closely correlated with an increase in interleukin-6 and terminal complement complex, reaching maximum 2 days after PCI; (2) C-reactive protein 2 days after PCI was significantly correlated with infarct size and parameters of LV remodelling 2 months after PCI; (3) Patients with persistent MO had significantly higher C-reactive protein levels 2 days following PCI. Conclusion We suggest that the rapid increase in C-reactive protein levels in this model of successful revascularization of a single, totally occluded vessel reflects the degree of inflammation within the infarcted area. Our findings support a role for C-reactive protein-mediated complement activation as both a marker and mediator of myocardial damage following MI. Clinical study no.: NCT 00465868.
Myocardial CCN2/CTGF is induced in heart failure of various etiologies. However, its role in the pathophysiology of left ventricular (LV) remodeling after myocardial infarction (MI) remains ...unresolved. The current study explores the role of CTGF in infarct healing and LV remodeling in an animal model and in patients admitted for acute ST-elevation MI.
Transgenic mice with cardiac-restricted overexpression of CTGF (Tg-CTGF) and non-transgenic littermate controls (NLC) were subjected to permanent ligation of the left anterior descending coronary artery. Despite similar infarct size (area of infarction relative to area at risk) 24 hours after ligation of the coronary artery in Tg-CTGF and NLC mice, Tg-CTGF mice disclosed smaller area of scar tissue, smaller increase of cardiac hypertrophy, and less LV dilatation and deterioration of LV function 4 weeks after MI. Tg-CTGF mice also revealed substantially reduced mortality after MI. Remote/peri-infarct tissue of Tg-CTGF mice contained reduced numbers of leucocytes, macrophages, and cells undergoing apoptosis as compared with NLC mice. In a cohort of patients with acute ST-elevation MI (n = 42) admitted to hospital for percutaneous coronary intervention (PCI) serum-CTGF levels (s-CTGF) were monitored and related to infarct size and LV function assessed by cardiac MRI. Increase in s-CTGF levels after MI was associated with reduced infarct size and improved LV ejection fraction one year after MI, as well as attenuated levels of CRP and GDF-15.
Increased myocardial CTGF activities after MI are associated with attenuation of LV remodeling and improved LV function mediated by attenuation of inflammatory responses and inhibition of apoptosis.
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.
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