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

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.
 ...
PMID:Cardiac troponin I levels in patients with left heart failure and cor pulmonale. 1138 82

We prospectively evaluated whether the combination of admission measurements of a marker for myocardial cell injury and a marker for left ventricular overload would effectively risk stratify patients with acutely decompensated heart failure. We measured serum concentrations of cardiac troponin T (cTnT) using a second-generation assay, as well as serum cardiac troponin I (cTnI) and plasma atrial and brain natriuretic peptide (BNP) concentrations on admission in 98 consecutive patients hospitalized for worsening chronic heart failure (mean age 69 years; 5 patients were in New York Heart Association functional class II, 35 were in class III, and 58 patients were in class IV). During a mean follow-up period of 451 days, there were 37 cardiac events, including 21 cardiac deaths (14 in-hospital deaths) and 16 readmissions for worsening heart failure. In a stepwise Cox regression analysis, including these biochemical markers, age, sex, functional class, and left ventricular ejection fraction, cTnT, and BNP were found to be significantly independent predictors of both cardiac death (p <0.05) and cardiac events (p <0.01). A cTnT >0.033 microg/L and/or a BNP >440 pg/ml on admission was correlated with an incremental increase in in-hospital cardiac mortality, overall cardiac mortality, and cardiac event rate. Kaplan-Meier analysis revealed that this combination could reliably stratify the patients into low-, intermediate-, and high-risk groups for cardiac events. Measuring the combination of admission concentrations of cTnT and BNP may be a highly effective means of risk stratification of patients hospitalized for worsening chronic heart failure.
 ...
PMID:Risk stratification using a combination of cardiac troponin T and brain natriuretic peptide in patients hospitalized for worsening chronic heart failure. 1189 11

Protein kinase C (PKC)-mediated phosphorylation of cardiac myofilament (MF) proteins has been shown to depress the actomyosin interaction and may be important during heart failure. Biochemical studies indicate that phosphorylation of Ser(43) and Ser(45) of cardiac troponin I (cTnI) plays a substantial role in the PKC-mediated depression. We studied intact and detergent-extracted papillary muscles from nontransgenic (NTG) and transgenic (TG) mouse hearts that express a mutant cTnI (Ser43Ala, Ser45Ala) that lacks specific PKC-dependent phosphorylation sites. Treatment of NTG papillary muscles with phenylephrine (PE) resulted in a transient increase and a subsequent 62% reduction in peak twitch force. TG muscles showed no transient increase and only a 45% reduction in force. There was a similar difference in maximum tension between NTG and TG fiber bundles that had been treated with a phorbol ester and had received subsequent detergent extraction. Although levels of cTnI phosphorylation correlated with these differences, the TG fibers also demonstrated a decrease in phosphorylation of cardiac troponin T. The PKC-specific inhibitor chelerythrine inhibited these responses. Our data provide evidence that specific PKC-mediated phosphorylation of Ser(43) and Ser(45) of cTnI plays an important role in regulating force development in the intact myocardium.
 ...
PMID:alpha-Adrenergic response and myofilament activity in mouse hearts lacking PKC phosphorylation sites on cardiac TnI. 1200 51

Despite considerable advances in medicine, the incidence of heart failure remains high in patients after myocardial infarction (MI). This study investigated the effects of engrafted early-differentiated cells (EDCs) from mouse embryonic stem cells, with or without transfection of vascular endothelial growth factor (VEGF) cDNA (phVEGF(165)), on cardiac function in postinfarcted mice. EDCs were transfected with green fluorescent protein (GFP) cDNA and transplanted into infarcted myocardium. Compared with the MI mice receiving cell-free medium, cardiac function was significantly improved in the MI mice 6 wk after transplantation of EDCs. Moreover, improvement of heart function was significantly greater in the mice implanted with EDCs overexpressing VEGF (EDCs-VEGF) than with EDCs alone. Frozen sections of infarcted myocardium with EDCs or EDCs-VEGF transplantation showed GFP-positive tissue. The area with positive immunostaining for cardiac troponin I and alpha-myosin heavy chain was larger in injured myocardium with EDCs or EDCs-VEGF transplantation than with medium injection. Transplantation of EDCs or EDCs-VEGF significantly increased the number of blood vessels in the MI area. However, the density of capillaries was significantly higher in the EDCs-VEGF animals than in the EDC mice. Double staining for GFP and connexin-43 was positive in injured myocardium with EDC transplantation. Our data demonstrate that engrafted EDCs or EDCs-VEGF regenerated cardiac tissue and significantly improved cardiac function in postinfarcted hearts. The novel EDCs-VEGF synergistic approach may have an important impact on future cell therapy for patients experiencing MI or heart failure.
 ...
PMID:VEGF enhances functional improvement of postinfarcted hearts by transplantation of ESC-differentiated cells. 1218 12

Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05-10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2 = .354; P = .009) but not with the diastolic thickness of the interventricular septum (P = .8467) or the left atrium: aorta ratio (P = .0652). Furthermore, cats with congestive heart failure at the time of cTnI analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P = .0095 and P = .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM.
 ...
PMID:Cardiac troponin I in feline hypertrophic cardiomyopathy. 1232 6

Cardiac troponin(cTn) is a sensitive marker for acute myocardial infarction(AMI). However, some cases of renal failure have been reported to show false positive results for cardiac troponin T(cTnT). Recently, it has been reported that heart-type fatty acid-binding protein(H-FABP) is a sensitive marker for AMI in the early phase. We evaluated the usefulness of cardiac troponin I(cTNI) using serum samples from patients(age 57-96) confirmed to have AMI with chest pain(n = 48), unstable angina pectoris(n = 11), cardiac failure(n = 5), others with high creatine phosphokinase(CK) activity(n = 81) and renal failure(n = 28), by comparing among cTnT(qualitative and quantitative), H-FABP, CK and creatine phosphokinase isoenzyme MB(CK-MB) activity. The diagnostic validity of cTn was assessed by receiver operating characteristic(ROC) curve analysis. The cut off value for AMI of cTnI was 0.8 ng/ml, cTnT was 0.16 ng/ml and H-FABP was 19.0 ng/ml. The overall diagnostic sensitivity of cTnI was 83.1%, and 84.8% for cTnT (quantitative), 72.3% for cTnT(qualitative), 64.8% for H-FABP, 81.8% for CK and 59.3% for CK-MB. The overall diagnostic specificity of cTnI was 90.9%, and 81.3% for cTnT(quantitative), 60.5% for cTnT (qualitative), 53.2% for H-FABP, 52.9% for CK and 87.7% for CK-MB. The overall diagnostic efficiency of cTnI was 86.5%, and 82.7% for cTnT(quantitative), 63.6% for cTnT(qualitative), 59.8% for H-FABP, 69.0% for CK and 71.9% for CK-MB. False positive results for cTnI were found in a few cases with renal failure. cTnT(qualitative) showed false positive results in 22/28 with serum creatinine over 2.1 mg/dl due to renal failure. In conclusion, cTnI detection is considered a useful and sufficiently sensitive marker for AMI.
 ...
PMID:[Usefulness of cardiac troponin I in patients with acute myocardial infarction]. 1245 79

Cardiac contusion is usually caused by blunt chest trauma and therefore is frequently suspected in patients involved in car or motorcycle accidents. The diagnosis of a myocardial contusion is difficult because of non-specific symptoms and the lack of an ideal test to detect myocardial damage. Cardiac contusion can cause life threatening arrhythmias and cardiac failure. Many diagnostic methods, such as ECG, biochemical cardiac markers, transthoracic and transoesophageal echocardiography, and radionuclide imaging studies, have been investigated to determine their use in predicting such complications. Recently, cardiac troponin I and T were found to be highly sensitive for myocardial injury. Troponin I and T have also proved to be useful in the stratification of patients at risk for complications. Nevertheless, diagnosis of a cardiac contusion and identification of patients at risk remain a challenge. In this review the current diagnostic tests will be discussed. Also, based on these diagnostic tests, a screening strategy containing data from the latest studies is presented, with the intention of detecting patients at risk.
 ...
PMID:Diagnosing cardiac contusion: old wisdom and new insights. 1269 46

Despite significant advances in medical therapy, patients with heart failure remain at increased risk of overall mortality, progressive ventricular dysfunction, and sudden cardiac death. Although a number of individual clinical and laboratory variables have been identified as being associated with increased mortality risk in heart failure, there remains a clear need for an integrated, accurate method of determining prognosis. Elevated plasma B-type natriuretic peptide (BNP) has been demonstrated to be a powerful marker for prognosis and risk stratification in the setting of heart failure. Patients with elevated BNP levels have been shown to be at significantly higher risk for heart failure admission or death, and higher BNP levels are associated with progressively worse prognosis. Although cardiac troponins are a well-established diagnostic and prognostic marker in acute coronary syndromes, emerging data suggest that cardiac troponins also provide independent prognostic information in heart failure. Detection of cardiac troponins in the serum of patients with heart failure has been shown to be associated with an impaired hemodynamic profile, progressive decline in left ventricular systolic function, and shortened survival. Combining a marker of myocyte injury-cardiac troponin-with BNP in a multimarker strategy appears to be a useful tool for improving risk assessment and triage in patients with heart failure. Heart failure patients with detectable cardiac troponin I and high BNP levels have been shown to have a 12-fold increased mortality risk compared with those with both undetectable cardiac troponin I and lower BNP. Integrating this multimarker approach into the routine assessment of heart failure patients will allow clinicians to more accurately identify high-risk patients who may derive increased benefit from intensive management strategies.
 ...
PMID:Combining natriuretic peptides and necrosis markers in determining prognosis in heart failure. 1456 25

Idiopathic dilated cardiomyopathy is a common cause of heart failure. Half of cases are believed to be hereditary, and mutations in cardiac sarcomeric contractile protein genes have been reported with autosomal dominant inheritance. We used mutation analysis suitable for identification of both dominant and recessive mutations to investigate the sarcomeric gene for cardiac troponin I (TNNI3) in 235 patients with dilated cardiomyopathy. We identified a novel TNNI3 mutation in a family with recessive disease. Functional studies showed impairment of troponin interactions that could lead to diminished myocardial contractility. TNNI3 is the first recessive gene identified for this condition, and we suggest that other such genes could be pinpointed by mutation analyses designed to identify homozygous mutations.
 ...
PMID:Novel mutation in cardiac troponin I in recessive idiopathic dilated cardiomyopathy. 1507 May 70

This review discusses the role of biochemical markers of myocyte injury in patients with chronic congestive heart failure. Heart specific assays have been developed for the measurement of cardiac troponin T (cTnT), cardiac troponin I (cTnI), heart type fatty acid binding protein (H-FABP), and myosin light chain 1 (MLC-1). Concentrations of these biochemical markers increase in the absence of ischaemic events in the subset of patients with heart failure whose long term outcomes are most adverse. The markers are easy to measure serially and it is therefore easy to follow patients without inter-observer variability. The serial clinical use of these markers, separately or in combination, will sharpen our understanding of the state of heart failure.
 ...
PMID:Biochemical markers of myocyte injury in heart failure. 1536 1


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>