Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent reports have demonstrated the presence of two isoforms of troponin I in the human fetal heart, namely, cardiac troponin I and slow skeletal muscle troponin I. Structural and physiological considerations indicate that these isoforms would confer differing contractile properties on the myocardium, particularly on the phosphorylation-mediated regulation of contractility by adrenergic agonists. We have investigated the developmental expression of these isoforms in the human heart from 9 weeks of gestation to 9 months of postnatal life, using Western blots revealed with troponin I antibodies to detect troponin protein isoforms and Northern blots to detect the corresponding mRNAs. The results show the following: 1) Slow skeletal muscle troponin I is the predominant isoform throughout fetal life. 2) After birth, the slow skeletal isoform is lost, with cardiac troponin I being the only isoform detectable by 9 months of postnatal development. 3) The protein isoforms and their corresponding mRNAs follow the same pattern of accumulation, suggesting that the transition in troponin expression is regulated at the level of gene transcription. The developmental transition in troponin I isoform content has implications for contractility of the fetal and postnatal myocardium. We further analyzed right and left ventricular muscle samples from 17 hearts in end-stage heart failure resulting from pulmonary hypertension, ischemic heart disease, or dilated cardiomyopathy. Cardiac troponin I mRNA remained abundant in each case, and slow skeletal muscle troponin I mRNA was not detectable in any of sample. We conclude that alterations in troponin I isoform content do not therefore contribute to the altered contractile characteristics of the adult failing ventricle.
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PMID:Troponin I gene expression during human cardiac development and in end-stage heart failure. 847 26

Cardiac troponin I, a specific and sensitive marker of myocardial damage, was detected in the blood of 6 of 26 patients studied in our Heart Failure Clinic. In these patients functional class, ventricular function, and prognosis were significantly worse than in those without detectable troponin I. This study suggests that troponin I may represent the biochemical marker of myocardial damage occurring in severe heart failure.
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PMID:Detectable serum troponin I in patients with heart failure of nonmyocardial ischemic origin. 920 29

Our objective was to evaluate the safety of coronary anastomosis on the beating heart by measuring the release of cardiac troponin I during minimally invasive coronary artery bypass grafting (MICABG). Cardiac troponin I (cTnI) is a reliable marker of cardiac ischemia during heart operations under cardiopulmonary bypass (CPB). Ten patients (8 males and 2 females, aged 41-63) underwent MICABG with single vessel bypass grafting for left anterior descending coronary artery (LAD) stenosis (n = 7) or occlusion (n = 3). Video-assisted surgery with left anterior minithoracotomy was performed in all patients. Serial venous blood samples were collected for measurement of cTnI before LAD occlusion (T0), during anastomosis (T1) and 10 min (T2), 6 h (T3), 24 h (T4), 48 h (T5), and 72 h (T6) after coronary reperfusion. The assay method used a specific enzyme-linked immunosorbent Stratus autoanalyzer. Control coronary angiography was performed in all patients. There were no operative complications or reoperations for bleeding. The cTnI concentrations were expressed in ng/ml +/- SD. The mean cTnI level was less than 3.05 +/- 0.2 ng/ml (range 0-32.8). Values were T0 = 0, T1 = 0.4 +/- 0.03, T2 = 1.15 +/- 0.2, T3 = 2.16 +/- 0.6, T4 = 1.5 +/- 0.3, T5 = 0.6 +/- 0.02, and T6 = 0.4 +/- 0.01. Angiography showed patent grafts in 9 patients. In one case, early internal thoracic artery (ITA) graft occlusion in a patient with 2 vessel disease was correlated with a higher cTnI concentration (17.8 ng/ml). Percutaneous angioplasty was performed on the right coronary artery, complicated with dissection and cardiac failure. This patient died 3 months after the MICABG despite support from a ventricular assist device. In conclusion, collateral circulation developed in the setting of chronic coronary occlusion may be efficient for myocardial preservation during short periods such as coronary anastomosis. cTnI immunoassay confirmed the safety of coronary anastomosis on the beating heart during minimally invasive coronary operations.
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PMID:Safety of beating heart anastomosis during video-assisted coronary surgery attested by cardiac troponin I. 965 Jun 74

Cardiac troponin I (cTnI) and creatine kinase MB isoenzyme (CK-MB) were measured in the plasma of 37 patients with acute heart failure. Elevated plasma cTnI concentrations were found in 89% of acute heart failure patients (P < 0.001 compared with a normal population), while plasma CK-MB showed no significant difference (P = 0.09). During follow-up, serial measurements of cTnI and CK-MB were performed. In acute heart failure patients, improvement of the clinical profile was associated with declining cTnI concentrations, while deterioration of heart function was closely related to increasing cTnI. Plasma CK-MB activities remained within the normal range throughout the observation period. This preliminary study provides evidence of cardiac damage to functionally overloaded myocytes. cTnI may be a sensitive marker both for early detection of myocyte damage and for monitoring of function in patients with acute heart failure.
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PMID:Monitoring of cardiac troponin I in patients with acute heart failure. 1045 4

Cardiac troponin levels are regarded as the most specific of currently available biochemical markers of myocardial damage. Elevated levels of troponin have been previously reported in patients with left heart failure, reflecting small areas of undetected myocardial cell death. The aim of this study was to compare the levels of the cardiac troponin I (cTnI) in patients with left- and right-sided heart failure. Cardiac troponin I levels were studied with immunochemical methods in patients with right heart failure (n = 17) resulting from chronic obstructive pulmonary disease, ischemic left heart failure (n = 23), and nonischemic left heart failure (n = 18) who were admitted to departments of cardiology and chest diseases. Also, cTnI levels were measured in 32 healthy subjects as control group. Protein markers of myocardial injury (cTnI and myoglobin) in patients with left and right heart failure were collected approximately 12 to 36 hours after onset of obvious symptoms. Serum creatine kinase MB band was determined on admission and thereafter twice a day during the first 3 days. Elevated levels of serum cTnI were found in patients with nonischemic (0.83 +/- 0.6 ng/mL, p<0.01) and ischemic left heart failure (0.9 +/- 0.5 ng/mL, p<0.01) when compared to healthy subjects, whereas serum cTnI levels in patients with right heart failure due to chronic obstructive pulmonary disease were not significantly different from those of control subjects (0.22 +/- 0.1 vs 0.16 +/- 0.1 ng/mL, p>0.05). In addition, creatine kinase MB band and myoglobin levels were not significantly different between patient and healthy groups. The mean of cTnI levels in ischemic and even nonischemic left heart failure were increased compared to the mean of values in healthy individuals but without significant creatine kinase MB band and myoglobin elevations. But cTnI levels were not increased in patients with right heart failure due to chronic obstructive pulmonary disease. These data indicate that the cTnI levels are abnormal in left heart failure but not in cor pulmonale.
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PMID:Cardiac troponin I levels in patients with left heart failure and cor pulmonale. 1138 82

Cardiac troponin I levels are frequently above normal values in several disease states in which myocardial necrosis is not a prominent aspect, particularly in pulmonary embolism, heart failure, liver cirrhosis, septic shock, renal failure and arterial hypertension. Sub-clinical myocardial necrosis has been postulated to be the cause of the phenomenon. Studies performed so far have not included pathological data to confirm this hypothesis. Increased troponin I plasma levels may be the result of myocardial strain, especially the type of strain that accompanies some forms of cardiac dilatation or hypertrophy. Troponin I may act as a marker of myocardial strain, either acute (in pulmonary embolism, septic shock and acute heart failure) or chronic (in chronic cardiac, renal and hepatic failure, as well as in arterial hypertension). The apparent paradox of elevated levels of troponin I without elevated levels of creatine kinase in several disease states might be solved if troponin I could be released from myocardial cells without the disruption of myocardial cell plasma membranes. Precise pathological studies are needed to elucidate whether increased troponin I with normal CK is associated with myocyte death, and, if so, with necrosis or with apoptosis.
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PMID:Cardiac troponin I in systemic diseases. A possible role for myocardial strain. 1158 28

Cardiac troponin I (cTnI) is a key regulatory protein in cardiac muscle contraction and relaxation, linking Ca(2+)-troponin C binding with activation of crossbridge reactions with the thin filament. In recent years, it has become increasingly apparent that myofilament properties as well as changes in intracellular Ca(2+) have a major role in the dynamic modulation of contractile function. The phosphorylation of specific serine and threonine residues on cTnI by several different kinases represents a major physiological mechanism for alteration of myofilament properties. Furthermore, altered thin filament function plays an important role in the contractile dysfunction associated with heart failure. Modification of cTnI by protein kinases A and C has been extensively studied with especially useful information deriving from (a) in vitro studies in reconstituted detergent-skinned fibre bundles in which endogenous cTnI was replaced with various targeted cTnI mutants and (b) transgenic animals in which endogenous cTnI was similarly manipulated through overexpression of cardiomyocyte-targeted cTnI mutants. cTnI may also be specifically modified by protein kinase G, p21-activated kinases and by dephosphorylation. This review focuses on recent advances in understanding the mechanisms of cTnI modification by these kinases and the consequent functional effects both under physiological conditions and in pathophysiological settings.
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PMID:Regulation of cardiac contractile function by troponin I phosphorylation. 1576 44

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are valuable heart markers in patients presenting with symptoms of ischaemic heart disease. A number of categories of patients frequently have raised concentrations of cardiac troponin (cTn) without having ischaemic heart disease. These include patients with heart diseases such as heart failure, myocarditis and valvular disease but also those with lung emboli, renal failure and sepsis. Possible underlying mechanisms are diffuse necrosis, cTn proteolysis or leakage of cytoplasmatic cTn with no irreversible damage to the contraction complex of heart-muscle cells. It is possible that cTn-measurement in patients with non-cardiac conditions is of prognostic value but so far this has only been demonstrated in dialysis patients and patients with pulmonary embolism.
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PMID:[The significance of elevated troponin levels in the absence of acute cardiac ischaemia]. 1661 May 13

Congestive heart failure is the one of the major cardiovascular disorder that is increasing in incidence and cause of death globally. Mortality rate has increased 40%-50% in advanced cardiac failure and 15%-25% in mild to moderate cardiac failure within one year of diagnosis. There is no established biochemical marker for the diagnosis, prognosis and staging of heart failure. Cardiac Troponin I may be a novel useful tool in identifying patients with Heart failure who are at increased risk for progressive ventricular dysfunction and death. Thirty six congestive heart failure cases and thirty six healthy controls were included in this study and serum cardiac troponin I and Ejection fraction were measured. All the study subjects were grouped according to the NYHA class they belong. Cardiac troponin I was significantly higher in CHF cases than the controls. Troponin I also significantly differed among groups. EF of cases was significantly lower than the controls and also differed among groups. A significant negative correlation between cardiac troponin I and progressive decline of ejection fraction was evident in this study. Cardiac troponin I increased progressively with progression of heart failure. Thus, Cardiac troponin I could be used to stratify patients undergoing heart failure in to high and low risk groups for future cardiac events. Cardiac troponin I could also be used as a very important marker for the prognosis of the patients with congestive heart failure.
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PMID:Role of cardiac troponin I in staging and prognosis of congestive heart failure subjects. 1734 72

Cardiac troponin I (TnI) knockout mice exhibit a phenotype of sudden death at 17-18 days after birth due to a progressive loss of TnI. The objective of this study was to gain insight into the physiological consequences of TnI depletion and the cause of death in these mice. Cardiac function was monitored serially between 12 and 17 days of age by using high-resolution ultrasonic imaging and Doppler echocardiography. Two-dimensional B-mode and anatomical M-mode imaging and Doppler echocardiography were performed using a high-frequency ( approximately 20-45 MHz) ultrasound imaging system on homozygous cardiac TnI mutant mice (cTnI(-/-)) and wild-type littermates. On day 12, cTnI(-/-) mice were indistinguishable from wild-type mice in terms of heart rate, atrial and LV (LV) chamber dimensions, LV posterior wall thickness, and body weight. By days 16 through 17, wild-type mice showed up to a 40% increase in chamber dimensions due to normal growth, whereas cTnI(-/-) mice showed increases in atrial dimensions of up to 97% but decreases in ventricular dimensions of up to 70%. Mitral Doppler analysis revealed prolonged isovolumic relaxation time and pronounced inversion of the mitral E/A ratio (early ventricular filling wave-to-late atrial contraction filling wave) only in cTnI(-/-) mice indicative of impaired LV relaxation. cTnI(-/-) mouse hearts showed clear signs of failure on day 17, characterized by >50% declines in cardiac output, ejection fraction, and fractional shortening. B-mode echocardiography showed a profoundly narrowed tube-like LV and enlarged atria at this time. Our data are consistent with TnI deficiency causing impaired LV relaxation, which leads to diastolic heart failure in this model.
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PMID:Progressive troponin I loss impairs cardiac relaxation and causes heart failure in mice. 1752 46


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