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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several recent epidemiologic studies investigating the short-term effects of particulate matter (PM) concentrations have shown carbon monoxide (CO) to have the strongest and most consistent statistical relationship with hospital admissions for cardiac diseases. This article suggests a potential hypothesis for these epidemiologic observations. Oxygen (O2) is transported, in reversible combination with hemoglobin, from the lungs to the tissues, where it diffuses into cardiac myocytes. Within the myocyte a portion of the O2 diffuses directly to the mitochondria, while the remaining O2 is transported by facilitated diffusion bound to myoglobin, a heme protein found in muscle. Within the mitochondria, O2 reacts to produce adenosine triphosphate (ATP), a high-energy phosphate compound that provides energy for all cell functions. Accordingly, the sustained production of ATP depends on the continuous delivery of O2 to the mitochondria, and failure at any point in the O2 transport system will compromise ATP production and myocardial function. Myoglobin, a fundamental constituent of cardiac muscle is essential for delivering O2 to the mitochondria. Myoglobin concentrations in cardiac tissue were 50% lower in patients with heart failure than in patients dying from noncardiac causes. Myoglobin concentrations are also severely depressed in animal models of congestive heart failure. Consequently, the role of myoglobin as a cellular transporter of O2 is seriously impaired by heart disease. Carbon monoxide reduces O2 transport to the tissues and, within the tissues, binds with myoglobin to form carboxymyoglobin (COMb). Thus, in cardiac patients CO further exacerbates the disease-related loss of myoglobin function. This further disrupts O2 transport and promotes adverse consequences for the compromised heart. Moreover, during hypoxia CO has the propensity of leaving the blood and binding with myoglobin in the intracellular compartment. Elderly persons with preexisting cardiopulmonary disorders appear to be at maximum risk of harmful health effects due to ambient air pollution exposure. Many of these disorders result in generalized or regional hypoxia. It is reasonable to hypothesize that CO also moves out of the blood of these patients and into the heart tissue whenever they are under hypoxic stress, such as exercise. Accordingly, CO binds with the marginal myoglobin concentrations present in the hearts of cardiac patients and further compromises cardiac function, resulting in poor tolerance of activity. Therefore, reduced cardiac myoglobin in people with heart disease, further exacerbated by CO moving into the cardiac tissue during episodes of hypoxia, may account for the positive association between ambient CO concentrations and hospitalization for heart disease.
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PMID:Biological plausibility for carbon monoxide as a copollutant in PM epidemiologic studies. 1288 88

Endomyocardial biopsy (EMB) is currently the standard method to diagnose acute graft rejection. However, considering the potential complications of this procedure, a noninvasive marker of rejection would be an ideal alternative or at least a helpful adjunct to posttransplant management. We measured myoglobin (Myo), creatine kinase MB mass (CK-MBm), troponin T (cTnT), serum amyloid A (SAA), and C-reactive protein (CRP) in 57 patients (mean age 37.5 years) who underwent orthotopic heart transplantation for end-stage cardiac failure between January and December 2001.Endomyocardial biopsies were performed routinely after surgery and histologically diagnosed rejection was graded according to the criteria of the International Society of Heart and Lung Transplantation. Concomittant with the biopsies, blood samples were drawn from the coronary sinus (central blood samples) and from a peripheral vein (peripheral blood samples) to assay biochemical markers. Among 149 EMB evaluated, 87 were negative (grade 0); 28 showed grade 1a rejection; 26 showed grade 1b; and 8 showed grade > 1b (2 were grade 2, 6 were grade 3a). Grades 0 and 1a were considered to be negative, while grades 1b and >1b were considered positive indicating potential acute graft rejection. cTnT, Myo, CK-MBm, SAA, and CRP levels were measured in 149 central blood samples and 149 peripheral blood samples. Myo and CK-MBm did not show significant changes. cTnT seems to be a potentially useful addition to the EMB results, while SAA and CRP showed variations with respect to EMB grade both in central and peripheral samples.
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PMID:Utility of biochemical markers in the follow-up of heart transplant recipients. 1469 83

Myoglobin plays various roles in oxygen supply to muscle mitochondria. It is difficult, and in some cases impossible, to study the relationship between the myoglobin concentration and the oxidative capacity of individual muscle cells because myoglobin has to be fixed in situ whereas determination of oxidative capacity, for example, succinate dehydrogenase activity, requires unfixed cryostat sections. We have investigated whether a vapour-fixation technique allows the use of serial sections to study the relationship between myoglobin and succinate dehydrogenase activity. The technique is used to study a rat soleus muscle, two human skeletal muscle biopsies and biopsies of two patients with chronic heart failure, and in a control and hypertrophied rat heart. Staining intensities were quantified by microdensitometry. The absorbance values were calibrated using sections cut from gelatine blocks containing known amounts of myoglobin. The results show that it is possible to use serial sections for the determination of the myoglobin concentration and succinate dehydrogenase activity, and indicate that myoglobin can lead to a substantial reduction (18-60%) of the extracellular oxygen tension required to prevent an anoxic core in muscle cells.
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PMID:Determination of myoglobin concentration and oxidative capacity in cryostat sections of human and rat skeletal muscle fibres and rat cardiomyocytes. 1504 78

Myocyte loss and replacement fibrosis have been observed in patients with hypertrophic cardiomyopathy (HC) with heart failure. This study was designed to elucidate whether heart-type fatty acid-binding protein (H-FABP), a sensitive biochemical marker for myocardial damage, indicates ongoing myocardial damage in patients with HC. We studied 48 patients with HC and 17 control subjects. Patients with HC were divided into 2 groups according to the New York Heart Association (NYHA) functional class: NYHA I + II (n = 40) and NYHA III + IV (n = 8). Serum H-FABP and myoglobin levels were measured, and extent score was used to assess the extent of thallium-201 perfusion defect. Serum H-FABP levels were significantly higher in patients with HC than in control subjects (3.8 +/- 1.6 vs 2.6 +/- 0.7 ng/ml, p = 0.0032). Furthermore, serum H-FABP levels were significantly higher in NYHA III + IV than in NYHA I + II (5.2 +/- 1.3 vs 3.5 +/- 1.5 ng/ml, p = 0.0043). Serum myoglobin levels showed no significant difference among the 3 groups (control, 46.6 +/- 15.0 ng/ml; NYHA I + II, 55.5 +/- 26.4 ng/ml; NYHA III + IV, 65.1 +/- 33.6 ng/ml, p = 0.2115). Extent score correlated positively with serum H-FABP levels (r = 0.420, p = 0.0026) and negatively with fractional shortening (r = -0.542, p <0.0001). Increased H-FABP levels indicate ongoing myocardial damage, which could result in clinical deterioration in patients with HC.
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PMID:Circulating levels of heart-type fatty acid-binding protein and its relation to thallium-201 perfusion defects in patients with hypertrophic cardiomyopathy. 1590 39

For a long time, the diagnosis of an acute myocardial infarction (AMI) seen in outdoor patients, was only relying on ECG findings. For that reason a certain amount of patients suffering from an AMI showing an atypical or not contributive ECG had not been identified as such and in consequence did not benefit from any prehospital treatment or had not been admitted in coronary care unit (CCU). With the arrival of the biological bed side monitoring in the SAMU, it became possible to measure via TRIAGE Cardiac the biological parameters of an AMI (myoglobin, troponin Ic and CKMB) and so confirm or exclude the diagnosis in certain cases. Other markers became measurable, such as BNP (brain natriuretic protein) a marker for early detection of heart failure. This natriuretic peptide is used during hospitalisation as a prognostic value in acute coronary syndrome with no cardiac insufficiency associated. More recently a semi quantitative test CardioDetect using the early release of h-FABP (heart fatty acid binding) showed a better sensibility in the first hours after chest-pain onset in out-door patients. The experience of the use of these biological bed side tests in the prehospital phase is only recent, but already permits a better management of out door patients. The future of there employ is promising. The combined use of these different markers in out door patients will probably allow in the near future identifying high risk patients.
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PMID:[Value of biochemistry performed in pre-hospital cardiology]. 1637 7

Heart-type fatty acid-binding protein (H-FABP) is a 132 amino acids soluble protein, with general characteristics resembling myoglobin. Because of its low molecular weight (15 kd) and cytoplasmic location, it constitutes a biologic marker readily released into the circulation after myocardial injury. Despite the development of various immunoassays to measure H-FABP, few are currently easy to perform, quantitative and applicable in emergency. Most studies have shown the diagnostic sensitivity of H-FABP (i.e. its ability to detect the presence of a myocardial infarction) to be high, above that of myoglobin in patients presenting within 3 to 6 h of after the onset of chest pain. This superiority is attributable to an earlier and more rapid rise in H-FABP than in myoglobin. After thrombolysis, the serum concentrations of H-FABP peak at approximately 4 h after the onset of chest pain, and return to normal values within 24 h. Because of this rapid return of its blood concentration to baseline, H-FABP can contribute to an early biologic diagnosis of post-thrombolysis reperfusion and re-infarction. In absence of renal insufficiency, H-FABP also provides a reliable estimate of infarct size associated with ST segment elevation. When myocardial injury occurs after cardiac surgery, the second peak in H-FABP concentration precedes that of myoglobin, CK-MB or troponins. In addition, H-FABP peaks earlier and is more sensitive than troponins in the detection of subtle myocardial injury in patients presenting with acute coronary syndrome without ST segment elevation, and in patients with severe heart failure, thus offering early prognostic information. Limitations of H-FABP include a limited cardio-specificity, a narrow diagnostic window (20 to 30 h), and a nearly exclusive renal elimination.
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PMID:[Diagnostic and prognostic value of heart-type fatty acid-binding protein (H-FABP), an early biochemical marker of myocardial injury]. 1643 2

Translating research into clinical practice has been a challenge throughout medical history. From the present review, it should be clear that this is particularly the case for heart failure. As a consequence, public awareness of this disease has been disillusionedly low, despite its prognosis being worse than that of most cancers and many other chronic diseases. We explore how over the past 150 years since Ludwig and Marey concepts about the evaluation of cardiac performance in patients with heart failure have emerged. From this historical-physiologic perspective, we have seen how 3 increasingly reductionist approaches or schools of thought have evolved in parallel, that is, an input-output approach, a hemodynamic pump approach, and a muscular pump approach. Each one of these has provided complementary insights into the pathophysiology of heart failure and has resulted in measurements or derived indices, some of which still being in use in present-day cardiology. From the third, most reductionist muscular pump approach, we have learned that myocardial and ventricular relaxation properties as well as temporal and spatial nonuniformities have been largely overlooked in the 2 other, input-output and hemodynamic pump, approaches. A key message from the present review is that relaxation and nonuniformities can be fully understood only from within the time-space continuum of cardiac pumping. As cyclicity and rhythm are, in some way, the most basic aspects of cardiac function, considerations of time should dominate over any measurement of cardiac performance as a muscular pump. Any measurement that is blind for the arrow of cardiac time should therefore be interpreted with caution. We have seen how the escape from the time domain-as with the calculation of LV ejection fraction-fascinating though as it may be, has undoubtedly served to hinder a rational scientific debate on the recent, so-called systolic-diastolic heart failure controversy. Lacking appreciation of early relaxation abnormalities and inappropriate degrees of nonuniformities has, indeed, led to some unfortunate misunderstandings about the pathophysiologic time progression of heart failure, in particular, heart failure with compensated hemodynamic pump function (ie, with normal or preserved LV ejection fraction). We have seen that with the introduction of newer powerful diagnostic techniques, as, for example, TDI and MRI, to evaluate ventricular "muscular pump" function, this debate can now be held in a more serene physiologic context. These aspects will be elaborated further in subsequent chapter papers of this symposium. With ongoing stem and other cell-based therapies and future reductionistic insights into cardiac cellular performance, we foresee the emergence of a fourth simple-parallel school of thought viewing the heart as a network of communicating different cell types, that is, cardiomyocytes, endothelial cells, fibroblasts, neurons. In this postgenomic age with the introduction of the rapidly evolving discipline of in vivo molecular imaging techniques, we anticipate that novel measurements of cardiac performance in patients with heart failure will soon become available and complement biopsy and other already available cardiac cellular biomarkers (cardiac troponin I; creatine kinase-MB; myoglobin; BNP). Through the use of these novel biomarkers as a fourth diagnostic track in the evaluation of cardiac performance in patients with heart failure, we will soon be able to increasingly understand the behavior of the heart as a complex biologic system-in other words, how these "low-level" biologic functions and signal transduction pathways at a cellular level contribute to the above "high-level" or system-level approach of cardiac performance at the muscular, the hemodynamic, and the input-output pump system levels and, hopefully, how they could contribute to an early diagnosis of chronic heart failure, in patients.
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PMID:Cardiac dysfunction in heart failure: the cardiologist's love affair with time. 1708 77

(31)P MRS studies in humans have shown that an impairment of cardiac energetics is characteristic of heart failure. Although numerous transgenic mouse models with a heart-failure phenotype have been generated, current methods to analyze murine high-energy phosphates (HEPs) in vivo are hampered by limited spatial resolution. Using acquisition-weighted 2D (31)P chemical shift imaging (CSI) at 9.4 Tesla, we were able to acquire (31)P MR spectra over the entire thorax of the mouse with high spatial resolution in defined regions of the heart (the anterior, lateral, posterior, and septal walls) within a reasonable acquisition time of about 75 min. Analysis of a transgenic cardiomyopathy model (double mutant: cardiospecific inducible nitric oxide synthase (iNOS) overexpression and lack of myoglobin (tg-iNOS(+)/myo(-/-)) revealed that cardiac dysfunction in the mutant was associated with an impaired energy state (phosphocreatine (PCr)/adenosine triphosphate (ATP) 1.54 +/- 0.18) over the entire left ventricle (LV; wild-type (WT): PCr/ATP 2.06 +/- 0.22, N = 5, P < 0.05), indicating that in the absence of efficient cytosolic NO scavenging, iNOS-derived NO critically interferes with the respiratory chain. In vivo data were validated against (31)P MR spectra of perchloric acid extracts (PCr/ATP: 1.87 +/- 0.21 (WT), 1.39 +/- 0.17 (tg-iNOS(+)/myo(-/-), N = 5, P < 0.05). Future applications will substantially benefit studies on the cause-and-effect relationship between cardiac energetics and function in other genetically well-defined models of heart failure.
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PMID:In vivo 2D mapping of impaired murine cardiac energetics in NO-induced heart failure. 1713 21

Increased serum level of troponin-T and myoglobin has been recently reported to be related to cumulative anthracycline exposure. Left ventricular ejection fraction seems accurate in monitoring systolic function according to the latest version of Toxicity Criteria by chemotherapeutics 3.0. From January 2002, 20 patients with untreated advanced breast cancer received epirubicin (25 mg/m/week) and paclitaxel (80 mg/m/week) for 24 weeks. Troponin-T, myoglobin and biochemical serum enzymes circulating levels were measured immediately before and 4 h after epirubicin administration every week. Patients underwent electrocardiography and echocardiography at weeks 0, 8, 16 and 24. The number of courses administered was 352 (median 18, range 4-24). Epirubicin median dose administered was 600 mg/m and paclitaxel median dose administered was 1760 mg/m. Troponin-T never overcame the upper normal limit; one patient experienced troponin-T elevation without any clinical or instrumental sign of cardiac failure. Myoglobin never significantly increased with the exception of a patient who underwent several abdominal fluid drainages. Creatine kinase MB and C-reactive protein never moved outside the upper normal limit. No symptomatic cardiac event was recorded. In 55 performed echocardiograms at weeks 0, 8, 16 and 24, neither left ventricular ejection fraction nor early peak flow/atrial flow velocity registered any significant decrease. No troponin-T or myoglobin serum elevations and Left ventricular ejection fraction/early peak flow/atrial flow velocity changes were registered in our series of nonsymptomatic women during epirubicin/paclitaxel weekly chemotherapy in the absence of clinical cardiac toxicity. Longer follow-up is needed, however, to understand whether the troponin-T or myoglobin circulating level measurement is able to detect subclinical, early-stage doxorubicin-induced cardiotoxicity.
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PMID:Troponin-T and myoglobin plus echocardiographic evaluation for monitoring early cardiotoxicity of weekly epirubicin-paclitaxel in metastatic breast cancer patients. 1715 9

Oncologic patients often receive treatment which is potentially cardiotoxic. Cardiotoxic complications range from fairly mild (relatively benign arrhythmias) to life threatening conditions (ischemia/myocardial infarction, heart failure, cardiomyopathy). The toxic effect of chemotherapy drugs may impair the integrity of the sarcomere, cause the release of bioactive substances into both tissues and the circulatory system and, consequently, cause necrosis/apoptosis of myocytes. A marker of the scope and severity of damage to the myocardium can be assessed by measuring the levels of cardiac markers in the serum. Cardiologic research is currently focused on the identification of new biochemical markers with a high degree of specificity, sensitivity and predictive value that might be used in the timely detection of myocardial abnormalities. The informative value of currently measured cardiac markers (myoglobin, CK-MB mass, CK-MB, and partly CK) is insufficient. There is growing evidence of the usefulness ofnatriuretic peptides and cardiac troponins in the diagnosing and monitoring of early and late, clinical and subclinical cardiotoxiticy resulting from anti-tumour therapy. The article summarises clinical studies concerning the diagnosis and monitoring of cardiotoxicity with the use of natriuretic peptides and cardiac troponins in former oncological patients.
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PMID:[Cardiotoxicity of antracycline treatment in the light of new biochemical diagnostic options]. 1770 27


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