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)

Accelerated atherosclerosis can lead to an increased prevalence of coronary artery disease, heart failure, brain stroke and peripheral arterial disease. Thus, subjects with chronic renal failure are exposed to increased morbidity and mortality from cardiovascular events. A strong and pervasive link exists between kidney failure and cardiac disease. A variety of individual biomarkers have been evaluated and several have been found to successfully predict the outcome in patients with kidney disease. These include markers of myocardial necrosis, such as cardiac troponin T and I, markers of heart failure, such as B-type of natriuretic peptide and its associated inactive N-terminal fragment, markers of systemic inflammation--C-reactive protein, and an endogenous inhibitor of nitric oxide synthase-asymmetric dimethyl arginin. Increased concentrations of C-reactive protein, B-type of natriuretic peptide, asymmetric dimethyl arginine, and troponin predict a high risk of cardiovascular mortality as well as a mortality due to other causes in patients with chronic renal failure or end stage renal disease (Tab. 1, Ref. 33). Full Text (Free, PDF) www.bmj.sk.
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PMID:Cardiac biomarkers and chronic renal diseases. 1883 40

Anthracycline-induced cardiotoxicity can cause serious health problems for an increasing number of children surviving childhood malignancies. Early detection of cardiac failure is critically important for the prevention and management of anthracycline-induced cardiotoxicity. The aim of this research was to determine the role of biomarkers in the early detection of anthracycline-induced cardiotoxicity in children. A literature review is presented of studies regarding the use of the biomarkers B-type natriuretic peptide (BNP), N-terminal pro-BNP (NT-pro-BNP), cardiac troponin T (cTnT), and cardiac troponin I (cTnI) in relation with anthracycline-induced cardiotoxicity in children. Six of 14 studies in children showed a significant relation between elevated biomarkers BNP, NT-pro-BNP, and cTnT and cardiac dysfunction. Six studies, although small, suggest that BNP, NT-pro-BNP, and cTnT might be useful markers in the early detection of anthracycline-induced cardiotoxicity.
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PMID:The role of biomarkers in the early detection of anthracycline-induced cardiotoxicity in children: a review of the literature. 1885 Apr 78

A 71-year-old woman was admitted to our department because of acute myocarditis. She was ameliorated with conventional heart failure treatment, however she developed left ventricular dilatation and cardiac troponin T (cTnT) was elevated again to >1.0 ng/ml 6 month after the first admission. She was re-admitted because of recurrent decompensated heart failure in spite of conventional treatment. Right ventricular endomyocardial biopsy revealed active myocarditis. Immunosuppressive therapy with prednisolone and azathioprine improved her symptoms and left ventricular function accompanied by a striking decrease of cTnT levels. The decreased cTnT level indicated an effective response to immunosuppression early after the beginning of treatment. These findings suggested that it is possible to evaluate the response to immunosuppressive therapy by serial measurement of cardiac troponin.
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PMID:The importance of serial cardiac troponin measurement for evaluating the response to immunosuppressive therapy for myocarditis. 1892 90

The aims of this study were to compare the prognostic value of cystatin C over creatinine and the Modification of Diet in Renal Disease (MDRD) equation and to evaluate whether it provides complementary information to cardiac biomarkers in the risk stratification of an unselected cohort of patients with acute heart failure. Consecutive hospitalized patients with established diagnoses of acute heart failure were prospectively studied. Blood samples were collected on hospital arrival to determine cystatin C, cardiac troponin T, and N-terminal-pro-brain natriuretic peptide. Clinical follow-up was obtained, and the occurrence of mortality and/or heart failure readmission was registered. One hundred thirty-eight patients (median age 74 years, interquartile range 67 to 80; 54% men) were studied. During a median follow-up period of 261 days (interquartile range 161 to 449), 60 patients (43.5%) presented with adverse events. After multivariate adjustment, cystatin C, N-terminal-pro-brain natriuretic peptide, cardiac troponin T, New York Heart Association functional class III or IV, and diabetes mellitus were identified as independent predictors of mortality and/or heart failure readmission. In contrast to creatinine and the MDRD equation, the highest cystatin C tertile (>1.50 mg/L) was a significant independent risk factor for adverse events (hazard ratio 3.08, 95% confidence interval 1.54 to 6.14, p = 0.004). A multimarker approach combining cardiac troponin T, N-terminal-pro-brain natriuretic peptide, and cystatin C improved risk stratification further, showing that patients with 2 (hazard ratio 2.37, 95% confidence interval 1.10 to 5.71) or 3 (hazard ratio 3.64, 95% confidence interval 1.55 to 8.56) elevated biomarkers had a higher risk for adverse events than patients with no elevated biomarkers (p for trend = 0.015). In conclusion, in this unselected cohort, cystatin C was a stronger predictor of adverse events than conventional measures of kidney function. In addition, cystatin C offered complementary prognostic information to cardiac biomarkers and could help clinicians perform more accurate risk stratification of patients with acute heart failure.
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PMID:Complementary prognostic value of cystatin C, N-terminal pro-B-type natriuretic Peptide and cardiac troponin T in patients with acute heart failure. 1953 88

Hypertrophic cardiomyopathy (HCM) is the most common cardiovascular genetic disorder, and can result in heart failure and sudden death in the young. No mutation is identified in up to 50% of cases of HCM following comprehensive analysis of known causal genes, however standard methods overlook large deletions and duplications. The multiple ligation-dependent probe amplification method was used to screen for large deletions and duplications in the myosin-binding protein-C (MYBPC3) and cardiac troponin T (TNNT2) genes in patients with HCM. One novel 3 base pair deletion was identified in MYBPC3 in a severely affected patient; however this change was also found in an unaffected relative. No alterations in the TNNT2 gene were identified. In conclusion, large deletions and duplications do not appear to play a major role in the pathogenesis of HCM.
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PMID:The role of large gene deletions and duplications in MYBPC3 and TNNT2 in patients with hypertrophic cardiomyopathy. 1966 96

Neuregulin-1 (NRG1) is a potential therapeutic agent for the treatment of doxorubicin (Dox)-induced heart failure. NRG1, however, activates the erbB2 receptor, which is frequently overexpressed in breast cancers. It is, therefore, important to understand how NRG1, via erbB2, protects the heart against Dox cardiotoxicity. Here, we studied NRG1-erbB2 signaling in Dox-treated mice hearts and in isolated neonatal rat ventricular myocytes (NRVM). Male C57BL/6 mice were treated with recombinant NRG1 before and daily after a single dose of Dox. Cardiac function was determined by catheterization. Two-week survival was analyzed by the Kaplan-Meier method. Cardiac troponins [cardiac troponin I (cTnI) and cardiac troponin T (cTnT)] and phosphorylated Akt protein levels were determined in mice hearts and in NRVM by Western blot analysis. Activation of caspases and ubiquitinylation of troponins were determined in NRVM by caspase assay and immunoprecipitation. NRG1 significantly improved survival and cardiac function in Dox-treated mice. NRG1 reduced the decrease in cTnI, cTnT, and cardiac troponin C (cTnC) and maintained Akt phosphorylation in Dox-treated mice hearts. NRG1 reduced the decrease in cTnI and cTnT mRNA and proteins in Dox-treated NRVM. Inhibition of erbB2, phosphoinositide 3-kinase (PI3K), Akt, and mTOR blocked the protective effects of NRG1 on cTnI and cTnT in NRVM. NRG1 significantly reduced Dox-induced caspase activation, which degraded troponins, in NRVM. NRG1 reduced Dox-induced proteasome degradation of cTnI. NRG1 attenuates Dox-induced decrease in cardiac troponins by increasing transcription and translation and by inhibiting caspase activation and proteasome degradation of troponin proteins. NRG1 maintains cardiac troponins by the erbB2-PI3K pathway, which may lessen Dox-induced cardiac dysfunction.
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PMID:Neuregulin-1 attenuated doxorubicin-induced decrease in cardiac troponins. 1980 90

A 60-year-old woman was admitted with acute heart failure and was diagnosed as having primary systemic AL amyloidosis with cardiac involvement by endomyocardial biopsy. Electrophoresis revealed an IgG-lambda monoclonal component and amyloidosis was evident in the gastric and rectal mucosa. Her cardiac function at diagnosis was poor, including an ejection fraction of 59% and IVS of 19 mm, and serum cardiac troponin T (cTnT) was elevated (0.12 ng/ml). She was treated with melphalan-dexamethasone (Mel-Dex) therapy once a month. After more than a year, cardiac function and performance status were maintained, with decreasing levels of cTnT, indicating that Mel-Dex represents a feasible and effective therapeutic option for patients with AL amyloidosis with cardiac dysfunction.
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PMID:Effective and well tolerated treatment with melphalan and dexamethasone for primary systemic AL amyloidosis with cardiac involvement. 2000 42

For years, cardiac troponins (cTn) have been regarded as the preferred biomarkers for the diagnosis of myocardial infarction and for the risk stratification of patients with acute coronary syndromes, as well as for the selection of patients who need an early invasive strategy, and for the guidance of adjunctive pharmacological therapy. In addition, measurement of cTn has been found useful for detection of myocardial necrosis in conditions unrelated to myocardial ischemia including acute pulmonary embolism, myocarditis, heart failure, sepsis, and end-stage renal disease. In these conditions, an unfavorable prognosis is unequivocally associated with detectable concentrations of cTn.A major limitation of most currently available cTn assays is the lack of adequate precision, i.e., to measure cTn concentrations at the 99th percentile value with a coefficient of variation < 10%. As a consequence, many manufacturers have developed more sensitive cTn assays that now comply with precision criteria required by the Joint European Society of Cardiology/ American College of Cardiology/American Heart Association/World Heart Federation Task Force for the Redefinition of Acute Myocardial Infarction.Using assays with higher analytic sensitivity more patients will be seen in clinical practice with the high-sensitivity cardiac troponin T (TnThs) above the 99th percentile discriminator. The causes of these elevations may be due to acute, subacute and chronic cardiac disease such as heart failure or cardiomyopathies.
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PMID:Troponins and high-sensitivity troponins as markers of necrosis in CAD and heart failure. 2002 39

Persistent elevation of cardiac troponin T (cTnT) predicts an adverse clinical outcome in patients with chronic heart failure (HF), but the underlying mechanisms remain to be determined. We investigated the association between predischarge cTnT elevation and coexistent pathophysiology in patients with decompensated HF. Plasma cTnT levels were determined before discharge in 170 patients with decompensated HF. We divided the patients into a group that was positive for cTnT [cTnT(+) group, n = 40] and a group that was negative for cTnT [cTnT(-) group, n = 130]. Multivariate analysis showed that use of beta-blocker therapy (odds ratio [OR] = 0.236, P = 0.003), an elevated high-sensitivity C-reactive protein (hsCRP) level (OR = 3.731, P = 0.006), a high brain natriuretic peptide (BNP) level (OR = 3.570, P = 0.007), diabetes (OR = 3.090, P = 0.018), and anemia (OR = 2.330, P = 0.047) were independently associated with cTnT positivity. During a mean follow-up period of 441 days after discharge, total mortality (P < 0.001), cardiac death (P < 0.001), and exacerbation of HF requiring hospitalization (P = 0.007) were all more common in the cTnT(+) group than in the cTnT(-) group. Cox proportional hazards analysis showed that cTnT positivity was an independent predictor of total mortality (hazard ratio = 5.008, P = 0.004) in an age- and gender-matched model. Elevation of cTnT during convalescence was associated with lack of beta-blocker therapy, a high hsCRP level at discharge, a high BNP level at discharge, diabetes, and anemia, and a worse clinical outcome in patients with decompensated HF.
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PMID:Elevated troponin T on discharge predicts poor outcome of decompensated heart failure. 2051 49

Mutations in TNNT2, encoding cardiac troponin T, commonly shows early onset, aggressive dilated cardiomyopathy (DCM). This observation may influence the decision of whether to undertake clinical genetic testing for TNNT2 in later onset DCM. Further, the trigger for late onset DCM remains enigmatic. A 70-year-old woman, previously healthy with a left ventricular ejection fraction of 50%-55% at age 69, presented with DCM of unknown cause and a 4-month history progressive heart failure requiring cardiac transplantation. Clinical genetic testing revealed a novel TNNT2 R139H mutation but no relevant variants in 18 other DCM genes. Her explanted heart showed partial fatty replacement in the right ventricle. Sequencing for five arrhythmogenic right ventricular dysplasia genes was negative. Functional studies in porcine cardiac skinned fibers reconstituted with the mutant R139H troponin T protein showed decreased Ca(2+) sensitivity at pH 7, characteristic of DCM. Because fatty infiltration may acidify the myocellular environment, maximal force development examined at pH 6.5 was diminished, suggesting a possible environmental trigger. We conclude that the TNNT2 R139H mutation was likely to be disease causing. Further, later age of onset may not be relevant to exclude genetic testing for TNNT2 mutations.
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PMID:Late onset sporadic dilated cardiomyopathy caused by a cardiac troponin T mutation. 2097 21


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