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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mammalian heart is not known to regenerate following injury. Therefore, there is great interest in developing viable tissue-based models for cardiac assist. Recent years have brought numerous advances in the development of scaffold-based models of cardiac tissue, but a self-organizing model has yet to be described. Here, we report the development of an in vitro cardiac tissue without scaffolding materials in the contractile region. Using an optimal concentration of the adhesion molecule laminin, a confluent layer of neonatal rat cardiomyogenic cells can be induced to self-organize into a cylindrical construct, resembling a papillary muscle, which we have termed a cardioid. Like endogenous heart tissue, cardioids contract spontaneously and can be electrically paced between 1 and 5 Hz indefinitely without fatigue. These engineered cardiac tissues also show an increased rate of spontaneous contraction (chronotropy), increased rate of relaxation (lusitropy), and increased force production (inotropy) in response to epinephrine. Cardioids have a developmental protein phenotype that expresses both alpha- and beta-tropomyosin, very low levels of SERCA2a, and very little of the mature isoform of cardiac troponin T.
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PMID:Self-organization of rat cardiac cells into contractile 3-D cardiac tissue. 1557 89

This study examined whether, in 16 male subjects, a continuous increase in heart rate (HR) during 4 h of ergometry cycling relates to cardiac fatigue or cardiomyocyte damage. Serum cardiac troponin T (cTnT) was determined and echocardiographic assessment was carried out prior to and after 2 h of exercise, within 15 min of completing exercise and after 24 h. Left ventricular contractile function (end-systolic blood pressure-volume relationship [SBP/ESV]) and diastolic filling (ratio of early to late peak left ventricular filling velocities [E:A]) were calculated. During exercise HR was 132+/-5 beats min(-1) after 2 h and increased to 141+/-5 beats min(-1) (mean +/- SD; P<0.05), but there was no evidence of altered LV contractile function (SBP/ESV 39.0+/-5.1 mmHg cm(-1) to 36.5+/-5.2 mmHg cm(-1) and SBP/ESV was not correlated to maximal oxygen uptake (r(2)=0.363). In contrast, E:A decreased (1.82+/-0.32 to 1.48+/-0.30; P<0.05) and returned towards baseline after 24 h (1.78+/-0.28), and individual changes were correlated to maximal oxygen uptake (r(2)=0.61; P<0.05). Low levels of cTnT were detected in two subjects after 4 h of exercise that had normalised by 24 h of recovery. During prolonged exercise cardiovascular drift occurred with echocardiographic signs of a reduced diastolic function of the heart, especially in those subjects with a high maximal oxygen uptake.
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PMID:Cardiac drift during prolonged exercise with echocardiographic evidence of reduced diastolic function of the heart. 1576 37

For a further depiction of exercise-induced cardiac dysfunction, N-terminal pro-brain natriuretic peptide (NT-pro-BNP) and cardiac troponin T (cTnT) were measured in recreational cyclists (n = 29) during the Otztal Radmarathon 2004. In all subjects, NT-pro-BNP significantly increased from 28 +/- 21 to 278 +/- 152 ng/L immediately after the race (p <0.001), decreased again on the following day, and returned to baseline values 1 week later. The mean percentage increase in NT-pro-BNP was 1,128 +/- 803%. CTnT, negative in all subjects before the race, increased transiently in 13 athletes (45%), with levels ranging from 0.043 to 0.224 mug/L in 8 of them (28%). One day after competition, cTnT had normalized in all athletes. Because of the typical release of kinetics, the deflection of NT-pro-BNP is considered to be the adequate volume regulatory response of a hemodynamically stressed heart to prolonged strenuous exercise. The observed kinetics of cTnT substantiate a release from the free cytoplasmatic pool due to the half-life of cytosolic cTnT. In healthy cyclists, transient increases in NT-pro-BNP and cTnT are more likely to reflect cardiac fatigue than injury.
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PMID:Effect of competitive marathon cycling on plasma N-terminal pro-brain natriuretic peptide and cardiac troponin T in healthy recreational cyclists. 1612 5

The mechanisms underlying acute respiratory failure induced by respiratory loads are unclear. We hypothesized that, in contrast to a moderate inspiratory resistive load, a severe one would elicit central respiratory failure (decreased respiratory drive) before diaphragmatic injury and fatigue. We also wished to elucidate the factors that predict endurance time and peak tracheal pressure generation. Anesthetized rats breathed air against a severe load ( approximately 75% of the peak tracheal pressure generated during a 30-s occlusion) until pump failure (fall in tracheal pressure to half; mean 38 min). Hypercapnia and hypoxemia developed rapidly ( approximately 4 min), coincident with diaphragmatic fatigue (decreased ratio of transdiaphragmatic pressure to peak integrated phrenic activity) and the detection in blood of the fast isoform of skeletal troponin I (muscle injury). At approximately 23 min, respiratory frequency and then blood pressure fell, followed immediately by secondary diaphragmatic fatigue. Blood taken after termination of loading contained cardiac troponin T (myocardial injury). Contrary to our hypothesis, diaphragmatic fatigue and injury occurred early in loading before central failure, evident only as a change in the timing but not the drive component of the central respiratory pattern generator. Stepwise multiple regression analysis selected changes in mean arterial pressure and arterial Pco(2) during loading as the principal contributing factors in load endurance time, and changes in mean arterial pressure as the principal contributing factor in peak tracheal pressure generation. In conclusion, the temporal development of respiratory failure is not stereotyped but depends on load magnitude; moreover respiratory loads induce cardiorespiratory, not just respiratory, failure.
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PMID:Cardiorespiratory failure in rat induced by severe inspiratory resistive loading. 1713 35

The aim of this study was to examine cardiac dysfunction following ultra-endurance exercise in male athletes. Fourteen athletes (mean+/-SD, age 39+/-8 years) were evaluated before and after the European Championship in Triathlon 2003 using echocardiogram (ECG), cardiac markers [cardiac troponin T (cTnT) and pro-brain natriuretic peptide (pro-BNP)] and echocardiography. Conventional echocardiography techniques and new Doppler tissue imaging (DTI) modalities were applied before and immediately after the competition. Blood samples were drawn 1 week before, immediately after and 12-24 h post-competition. CTnT significantly increased immediately, but decreased to within normal limits 12-24 h post-competition. Pro-BNP was significantly increased immediately post-race (27+/-21 vs 7+/-2 pmol/L pre-race, P < or = 0.007), which 12-24 h later, decreased to 19+/-14 pmol/L (P = 0.07 vs pre-race). During echocardiography, no significant differences were found in regional or global systolic parameters. Early diastolic peak flow velocity (9+/-2, P = 0.04) and E/A ratio (2+/-1, P = 0.004) were increased pre-race and decreased significantly toward normal values. In one athlete, cTnT levels increased significantly and systolic velocities decreased, thus suggesting reversible cardiac fatigue. When using cardiac markers and echocardiographic findings, a triathlon was found to have no significant negative effects on left ventricular function or myocardial tissue in male athletes.
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PMID:Myocardial response to a triathlon in male athletes evaluated by Doppler tissue imaging and biochemical parameters. 1824 32

We measured analytes in collapsed Boston Marathon runners to compare with changes in asymptomatic runners. Of collapsed runners at the 2007 marathon, 18.2% had a measurable cardiac troponin T (cTnT) value with a mean postrace level of 0.017 ng/mL (0.017 microg/L; SD, 0.02 ng/mL [0.02 microg/L]). Three subjects had cTnT values above the cutoff (0.10 ng/mL [0.10 microg/L]) typically used for the diagnosis of acute myocardial infarction. The mean and median N-terminal pro-B-type natriuretic peptide levels were 73 ng/L (SD, 77.3 ng/L) and 54.3 ng/L (interquartile range, 22.8-87.3 ng/L), respectively, in collapsed runners. Only 4.9% had values more than the age-specific normal value (<125 ng/L for subjects younger than 75 years). In collapsed subjects at the 2006 marathon, 18.0% had an abnormal sodium value, including 18 cases of hypernatremia and 7 cases of hyponatremia. The ionized calcium level was low in 49% of subjects, and the ionized magnesium level was low in 19.5% and elevated in 1 subject. The blood lactate level was elevated in 95% of subjects. The frequency of elevated postrace cTnT levels in collapsed athletes after endurance exercise is similar to that in asymptomatic runners. Other metabolic abnormalities, including hypernatremia, hyponatremia, low ionized calcium and magnesium levels, and lactic acidosis may contribute to muscle fatigue and collapse.
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PMID:Cardiac biomarkers, electrolytes, and other analytes in collapsed marathon runners: implications for the evaluation of runners following competition. 1848 12

We previously showed that severe inspiratory resistive loads cause acute (<1 h) cardiorespiratory failure characterized by arterial hypotension, multifocal myocardial infarcts, and diaphragmatic fatigue. The mechanisms responsible for cardiovascular failure are unknown, but one factor may be the increased ventricular afterload caused by the large negative intrathoracic pressures generated when breathing against an inspiratory load. Because expiratory threshold loads increase intrathoracic pressure and decrease left ventricular afterload, we hypothesized that anesthetized rats forced to breathe against such a load would experience only diaphragmatic failure. Loading approximately doubled end-expiratory lung volume, halved respiratory frequency, and caused arterial hypoxemia and hypercapnia, respiratory acidosis, and increased inspiratory drive. Although hyperinflation immediately reduced the diaphragm's mechanical advantage, fatigue did not occur until near load termination. Mean arterial pressure progressively fell, becoming significant (cardiovascular failure) midway through loading despite tachycardia. Loading was terminated (endurance 125 +/- 43 min; range 82-206 min) when mean arterial pressure dropped below 50 mmHg. Blood samples taken immediately after load termination revealed hypoglycemia, hyperkalemia, and cardiac troponin T, the last indicating myocardial injury that was, according to histology, mainly in the right ventricle. This damage probably reflects a combination of decreased O(2) delivery (decreased venous return and arterial hypoxemia) and greater afterload due to hyperinflation-induced increase in pulmonary vascular resistance. Thus, in rats breathing at an increased end-expiratory lung volume, cardiorespiratory, not just respiratory, failure still occurred. Right heart injury and dysfunction may contribute to the increased morbidity and mortality associated with acute exacerbations of obstructive airway disease.
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PMID:Hyperinflation-induced cardiorespiratory failure in rats. 1940 48

A 55-year-old female presented with 4-day history of fatigue and exertional shortness of breath. A late presentation inferior ST elevation myocardial infarction (STEMI) was diagnosed based on ST elevation in the inferior leads of electrocardiography and elevated cardiac troponin T (TnT). She developed complete heart block 1 day after admission to the hospital and remained hemodynamically stable. She was taken to the catheterization laboratory for a temporary pacing wire insertion. Coronary angiogram at the same time showed an occluded right coronary artery at the mid-section. The lesion was successfully opened. Within 24 hours, the patient's heart rhythm returned to sinus with first-degree atrioventricular block (AVB), thus avoiding the need for a permanent pacemaker. Current guidelines recommend medical management for late presentation hemodynamically stable STEMI of more than 72 H onset. Current ACC/AHA/HRS Pacemaker Guidelines recommend reperfusion strategy for acute presentation inferior STEMI associated with AVB. However, no clear strategy exists in the case of late presentation inferior STEMI with advanced AVB. Our case report suggests that late coronary intervention could be a management strategy in such a scenario in order to avoid a permanent pacemaker.
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PMID:Complete heart block in late presentation of inferior STEMI successfully treated with percutaneous coronary intervention. 2189 17

A 53-year-old man with active hepatitis C and cirrhosis presented with a vasculitic rash, myalgias, and fatigue, and was found to have an elevated cardiac troponin I up to 15.7 ng/mL with normal electrocardiogram, echocardiogram, and coronary angiogram prior to being discharged. Subsequently, during a similar presentation to another academically affiliated hospital, the patient had a normal cardiac troponin T (< 0.01 ng/mL). Upon his third presentation with significantly elevated troponin I to 15.98 ng/mL, the patient was found to have cryoglobulinemic vasculitis and elevated rheumatoid factor due to active hepatitis C, causing interference with the troponin I immunoassay. In conclusion, troponin I assays may have high false-positive values due to interference by rheumatoid factor and/or a polyclonal antibody found in cryoglobulinemia.
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PMID:False-positive Troponin I Assay elevation due to occult Mixed Cryoglobulinemic Vasculitis. 3103 6