Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular disease today remains a formidable foe affecting 1 in 3 Americans. The emergence of cardiac biochemical markers has provided clinicians unique insight into the state of the myocardium. In fact, cardiac biomarkers now represent an essential criterion in the definition of acute myocardial infarction. There has been impressive development of efficient and reliable assays to detect biomarkers in the serum. Together with patient history and electrocardiographic analysis, the invaluable information gained from serum cardiac biomarkers supports diagnosis, therapy selection, and determination of prognosis. Biomarkers such as troponin and creatine kinase MB have received well-deserved attention for their ability to detect myocardial ischemia. Clinicians today use cardiac markers to identify ischemia as well as alternate clinical states. B-type natriuretic peptide, for instance, reflects myocardial stretch as seen in heart failure exacerbations and may well have promising prognostic significance. The purpose of this review is to discuss current and emerging cardiac biomarkers in acutely ill patients. The advantages and disadvantages of biomarkers will also be presented in the context of their clinical uses. Present markers are highly sensitive and specific to myocardial injury; however they do not specifically identify the method of injury. An exciting potential exists for future biomarkers to demonstrate enhanced specificity and earlier detection of compromised myocardium.
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PMID:Biomarkers in acute cardiovascular disease. 1838 55

The present study sought to identify confounding factors for the interpretation of copeptin levels in healthy individuals. The natriuretic peptides are recognized as diagnostic and prognostic tools in HF (heart failure). Interpretation of BNP (brain natriuretic peptide) and NTproBNP (N-terminal pro-BNP) levels is multifaceted as their secretion is influenced by many variables. A newly identified glycopeptide called copeptin is comparable with the natriuretic peptides in the diagnosis and prognosis of HF and as a prognostic biomarker after AMI (acute myocardial infarction). Copeptin, derived from the C-terminal portion of the precursor to AVP (arginine vasopressin), is secreted stoichiometrically with vasopressin, hence it can be used as a surrogate marker of the AVP system. In the present study, 706 healthy volunteers were recruited from a local HF screening study. Participants with a history of cardiovascular disease and those with echocardiographic abnormalities were excluded from the study. Copeptin and NTproBNP levels were assayed using in-house immunoluminometric assays. Median copeptin levels were significantly higher in the male volunteers compared with the females [median (range): 4.3 (0.4-44.3) compared with 3.2 (1.0-14.8) pmol/l; P<0.001]. In males, copeptin was correlated with eGFR (estimated glomerular filtration rate; r(s)=-0.186, P<0.001). In females, the correlation of copeptin with eGFR was weak (r(s)=-0.097, P=0.095). DT (deceleration time) and left atrial size correlated with higher copeptin levels (r(s)=0.085, P=0.029 and r(s)=0.206, P<0.001 respectively). Only gender (P<0.001), eGFR (P<0.001), left atrial size (P=0.04) and DT (P=0.02) remained independently predictive of plasma copeptin. The present study suggests that gender and renal function specific partition values should be used to interpret copeptin values in future studies of this biomarker in HF or ischaemic heart disease.
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PMID:Gender and renal function influence plasma levels of copeptin in healthy individuals. 1864 34

B-type natriuretic peptide (BNP) and its N-terminal fragment (NT-proBNP) are released from ventricular cardiomyocytes in response to an increase in ventricular wall stress and to myocardial ischemia. Both BNP and NT-proBNP have proven to be reliable diagnostic and prognostic biomarkers in patients with heart failure. Recently, the diagnostic roles of BNP and NT-proBNP in patients with coronary artery disease (CAD) have been investigated. For patients with acute coronary syndromes, data have been derived from a great number of studies, whereas in patients with stable CAD, only a limited amount of recent data is available; although limited, these data show that elevations in BNP and NT-proBNP levels are associated with the extent of CAD, thus providing prognostic information for an unfavourable clinical outcome. However, clinical and therapeutic implications are indistinct and need to be elucidated in further studies.
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PMID:B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide - Diagnostic role in stable coronary artery disease. 1865 Oct 43

Increasing lines of evidence has been accumulated that nitric oxide (NO) and nitric oxide synthase (NOS) distribute plentifully in the rostral ventrolateral medulla (RVLM) and contribute to cardiovascular regulation. In the present study, the expressions of neuronal and inducible isoform of NOS (nNOS and iNOS) were observed in the RVLM of acute myocardial ischemia (AMI) Wistar rats experienced electroacupuncture (EA) treatment, thereby the cardiovascular effects of NO in the RVLM were investigated and the mechanism of acupuncture effect on AMI was inferred. The results indicated that in the AMI rats, cardiac functions were markedly attenuated with high serum level of brain natriuretic peptide (BNP) and norepinephine (NE), the number of nNOS-immunoreactive cells and nNOS mRNA exprossion in the RVLM area were increased, while those of iNOS were lowered. EA at "Neiguan" acupoints (Pe 6) 30 min daily for successive 5 d resulted in an improvement of the cardiac functions, decreases in NE and BNP levels; it also increased the expression of iNOS and decreased the expression of nNOS in the RVLM. These results suggest that the curative effect of acupuncture on AMI is possibly attributable to the differential regulation of NOS/NO in the RVLM, leading to decreased sympathetic outflow and improvement of cardiac functions.
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PMID:Differential expressions of nNOS and iNOS in the rostral ventrolateral medulla induced by electroacupuncture in acute myocardial ischemia rats. 1869 Mar 86

Levels of natriuretic peptides, including B-type natriuretic peptide and N-terminal prohormone brain natriuretic peptide, are strong independent predictors of prognosis in acute coronary syndrome (ACS). They are associated with short- and long-term mortality and with the risk of new-onset heart failure, above and beyond the conventional risk factors. Myocardial ischemia and ventricular wall stress are triggers for the release of natriuretic peptides, and although the latter are associated with the severity of the underlying coronary artery disease, they fail to predict recurrent nonfatal ACS. In conclusion, natriuretic peptide values may improve risk stratification in ACS when used in addition to troponin levels and other prognostic markers, but more data are needed to define their role in ACS therapy.
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PMID:Natriuretic peptides in acute coronary syndromes: prognostic value and clinical implications. 1877 30

This study investigated plasma brain natriuretic peptide (BNP) levels in normotensive and hypertensive patients with suspected coronary artery disease during radionuclide pharmacological stress testing. Twenty-seven normotensive patients (15 males, aged 63.0+/-4.5 years and 12 females, aged 63.0+/-4.1 years) and 38 essential hypertensive patients (25 males, aged 63.3+/-3.3 years and 13 females, aged 64.6+/-2.6 years) with chest pain and exercise stress testing inconclusive for coronary artery disease underwent myocardial perfusion single-photon emission computed tomography (SPECT) using adenosine infusion. SPECT identified patients without (16 normotensive and 22 hypertensive) and patients with (11 normotensive and 16 hypertensive) transient perfusion defects. Basal BNP levels in normotensive patients without transient myocardial ischemia (3.1+/-1.2 fmol/ml) were significantly (P<0.01) lower than those observed in normotensive patients with transient ischemia (8.2+/-1.2 fmol/ml), whereas BNP levels in hypertensive patients without transient ischemia (8.2+/-1.0 fmol/ml) did not significantly differ from those in hypertensive patients with transient ischemia (8.1+/-2.0 fmol/ml). No significant difference was found in BNP levels between males or females either in normotensive or hypertensive patients without or with ischemia. Adenosine infusion did not significantly change BNP levels in any subject group without or with myocardial perfusion defects. Our findings show that increases in BNP allow early detection of myocardial ischemia in normotensive patients, but not in hypertensive patients with suspected coronary artery disease. Adenosine-induced myocardial ischemia does not affect BNP production already activated by coronary artery disease in normotensive patients and by hemodynamic changes in hypertensive patients.
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PMID:Plasma brain natriuretic peptide at rest and after adenosine-induced myocardial ischemia in normotensive and essential hypertensive patients with suspected coronary artery disease. 1895 35

Echocardiographic strain with strain rate imaging is a new technology enabling more reliable and comprehensive assessment of myocardial function. The spectrum of potential clinical applications is very wide due to its ability to differentiate between active and passive movement of myocardial segments, to quantify intraventricular dyssynchrony and to evaluate components of myocardial function, such as longitudinal myocardial shortening, that are not visually assessable. In-vivo and in-vitro validation of 2D-strain imaging technique have been undertaken and reached a point where it is considered ready for more widespread investigations into clinical utility, e.g. regarding myocarditis, arrhythmogenic right ventricular dysplasia/cardiomyopathy and regional ischemia. Moreover, longitudinal LV strain is closely related to log plasma brain-type natriuretic peptide levels in patients with congestive heart failure, both in patients with systolic and diastolic heart failure. We present a case of detection of coronary artery disease in a 55-year-old Italian man. This case focuses attention on the higher sensibility of the 2-Dimensional Strain echocardiography the diagnosis of myocardial ischemia in patients with coronary artery disease.
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PMID:2-Dimensional strain echocardiography and early detection of myocardial ischemia. 1918 69

Circulating levels of B-type natriuretic peptide (BNP) and the amino-terminal portion of the prohormone (NT-proBNP) have been reported to increase immediately after myocardial ischemia. The association between extent of exercise-induced myocardial ischemia measured using myocardial perfusion scintigraphy and the magnitude and time course of changes in NT-proBNP was studied. One hundred one patients underwent symptom-limited exercise myocardial perfusion scintigraphy. Myocardial ischemia was assessed semiquantitatively. Serum samples were obtained before the start of exercise (baseline), at maximal exercise, and every hour up to 6 hours after maximal exercise. Myocardial ischemia was present in 37 patients (37%). NT-proBNP rapidly increased during exercise (to 113%, interquartile range 104 to 144, and 118%, interquartile range 106 to 142, of baseline, respectively), with a second peak at 4 (141%, interquartile range 119 to 169) and 5 hours (136%, interquartile range 93 to 188), respectively. Absolute changes between NT-proBNP at baseline and at maximum exercise in patients with versus without ischemia were similar (median, 30 pg/ml, interquartile range 7 to 45 vs 15, interquartile range 4 to 46, respectively, p = 0.230), but absolute change between baseline and the secondary peak was higher in patients with ischemia than in patients without ischemia (median 64 pg/ml, interquartile range 32 to 172 vs 34, interquartile range 19 to 85, respectively, p = 0.024). In multivariate linear stepwise regression analysis of determinants of changes in NT-proBNP after exercise, baseline NT-proBNP was the only independent determinant of absolute changes at maximum exercise, whereas the presence of ischemia was not predictive. Baseline NT-proBNP, cystatin C, and end-systolic volume were independent determinants of the absolute increase to secondary peak levels. In conclusion, myocardial ischemia per se did not lead to additional increases in NT-proBNP within 6 hours after exercise.
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PMID:Relation of N-terminal pro B-type natriuretic peptide levels after symptom-limited exercise to baseline and ischemia levels. 1923 20

The insulin-like and vasodilatatory polypeptide relaxin (RLX), formerly known as a pregnancy hormone, has gained interest as a potential humoral mediator in human heart failure. Controversy exists about the relation between plasma levels of RLX and the severity of heart failure. The present study was designed to determine the course of RLX, atrial, and brain natriuretic peptide (NT-proANP and NT-proBNP) during physical exercise in patients with ischemic heart disease (IHD) and to relate hormone levels to peak cardiac power output (CPO) as a measure of cardiopulmonary function with prognostic relevance. 40 patients with IHD were studied during right-heart-catheterization at rest and during supine bicycle ergometry. RLX, NTproBNP, and NTproANP were determined before, during exercise, and after recovery. NT-proANP and NT-proBNP levels increased during maximal charge, and recovery while RLX levels decreased. Cardiac power output at maximal charge correlated inversely with NTproANP and NTproBNP but positively with RLX. Patients with high degree heart failure (CPO<1.96 W) had higher NTproANP and NTproBNP and lower RLX levels than patients with low degree heart failure. While confirming the role of NTproANP and NTproBNP as markers for the severity of heart failure, the present data do not support the concept that plasma levels of RLX are related to the severity of myocardial dysfunction and that systemic RLX acts as a compensatory vasodilatatory response hormone in ischemic heart disease.
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PMID:The effects of physical exercise on plasma levels of relaxin, NTproANP, and NTproBNP in patients with ischemic heart disease. 1938 Feb 80

B-type natriuretic peptide (BNP) is a peptide hormone of myocardial origin with significant cardioprotective properties. Patients with myocardial ischemia present with high levels of BNP in plasma and elevated expression in the myocardium. However, the molecular mechanisms of BNP induction in the ischemic myocardium are not well understood. The aim of the investigation was to assess whether myocardial hypoxia induces the production of BNP in human ventricular myocytes. To test the hypothesis that reduced oxygen tension can directly stimulate BNP gene expression and release in the absence of hemodynamic or neurohormonal stimuli, we used an in vitro model system of cultured human ventricular myocytes (AC16 cells). Cells were cultured under normoxic (21% O(2)) or hypoxic (5% O(2)) conditions for up to 48 h. The accumulation of BNP, atrial natriuretic peptide (ANP), and vascular endothelial growth factor (VEGF) was then measured. Hypoxia stimulated the protein release of BNP and VEGF but not ANP. In concordance, the increased mRNA levels of BNP and VEGF but not ANP were found on culturing AC16 cells under hypoxic conditions. The analysis of the transcriptional activity of the hypoxia-inducible factor 1 (HIF-1) in nuclear extracts showed that HIF-1 activity was induced under hypoxic conditions. Finally, the treatment of AC16 cells with the HIF-1 inhibitor rotenone in hypoxia inhibited BNP and VEGF release. In conclusion, these data indicate that hypoxia induces the synthesis and secretion of BNP in human ventricular myocytes, likely through HIF-1-enhanced transcriptional activity.
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PMID:Hypoxia induces B-type natriuretic peptide release in cell lines derived from human cardiomyocytes. 1954 90


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