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)

The prevalence of heart failure will increase in a number of industrialized countries as the proportion of elderly within the population increases. Despite recent advances in medical and surgical intervention, the prognosis for this disorder has not improved significantly. To make a major impact on the prognosis for heart failure, it would be important to be able to recognize various forms of heart disease before severe heart failure has developed. Chest X-radiography, ECG and echocardiography may not be adequate screening tools for heart failure in large populations. Natriuretic peptides are secreted from the heart in response to various cardiac abnormalities including ventricular dysfunction, volume overload, hypertrophy, and myocardial ischemia. Circulating levels of natriuretic peptides are elevated in various forms of structural cardiac disease regardless of etiology and the degree of ventricular systolic dysfunction. Natriuretic peptides, specifically B-type natriuretic peptide, are practically stable and can be measured without an extraction procedure. We have reviewed the recent status of plasma natriuretic peptide measurement for identification of patients with congestive heart failure, left ventricular dysfunction, and high risk of heart failure, especially in mass screening settings.
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PMID:Natriuretic peptide measurement as a screening test for overt and subclinical heart failure. 1460 11

Cardiac markers are now considered as useful indexes for the diagnosis of myocardial ischemia and prediction of future events. Measurements of creatine kinase (CK) and MB enzymes have been considered as the gold standard in the past, but they lack sensitivity and specificity. Troponin has progressively gained acceptance as the new standard. Troponin assay is now widely available and several authors have demonstrated its diagnostic accuracy, predictive value, and capacity to predict prognosis and guide therapy in acute coronary artery disease. Further evaluations have however opened the perspective of more sensitive markers which may also exhibit more prompt elevation. B-type natriuretic peptide (BNP) is secreted during myocardial ischemia in response to increased overload pressure. BNP rises immediately after ischemic events and may be more sensitive than other cardiac markers, including troponin. Moreover, new techniques allow immediate determination. BNP therefore would be of great interest for the diagnosis and management of myocardial ischemia. New markers may allow determination of coronary plaque fissuring and detection of coronary disease at a preclinical phase.
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PMID:[New biological markers for acute coronary artery disease]. 1497 29

Natriuretic peptides (BNP and NT-proBNP) have been shown to be useful tools for risk stratification of patients with acute myocardial ischemia encompassing the whole spectrum of acute coronary syndromes (ACS), particularly for prediction of mortality. Both BNP and NT-proBNP possess several characteristics of the ideal biomarker, showing independent and incremental prognostic value above traditional clinical, electrocardiographic, and biochemical (particularly troponin) risk indicators. Specifically, in ACS patients, BNP and NT-proBNP have powerful prognostic value both in patients without a history of previous heart failure or without clinical or instrumental signs of left ventricular dysfunction on admission or during hospital stay. They can also be easily and rapidly measured in an emergency context. We have performed a meta-analysis of available studies concerning the prognostic value of natriuretic peptides. Our results show that the prognostic value of natriuretic peptides is similar: (1) both at short- and long-term; (2) when natriuretic peptides are measured at first patient contact or during hospital stay; (3) for BNP or NT-proBNP; and (4) in patients with ST elevation myocardial infarction or no ST elevation ACS. These data suggest that natriuretic peptide measurement should be integrated into routine evaluation of patients with an ACS.
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PMID:Natriuretic peptides for risk stratification of patients with acute coronary syndromes. 1498 84

Plasma brain natriuretic peptide (BNP) levels have been associated with left ventricular dysfunction and acute myocardial infarction. Although natriuretic peptide responses have been linked to exercise-induced myocardial ischemia, it is not known whether BNP levels predict dobutamine-induced myocardial ischemia. The aim of this study was to determine whether elevations in BNP levels immediately before or after dobutamine-induced stress are associated with echocardiographic myocardial ischemia. Plasma BNP was measured before and after stress during dobutamine-stress echocardiography in 317 patients (aged 68 +/- 11 years; 46% women) who had creatinine <1.5 mg/dl and did not have valvular disease. Ischemia, as assessed by blinded echocardiographic interpretation, was noted in 31 patients (10%). In univariable analyses, prestress BNP was predictive of echocardiographic ischemia (rates of ischemia according to tertiles of BNP 4%, 9%, and 16%, chi-square for trend = 8, p = 0.0059). The change in BNP levels with dobutamine stress was not associated with ischemia. In multivariable analyses, after adjusting for age, gender, and left ventricular ejection fraction, BNP before and after stress remained predictive of ischemia (1 SD increase in the log of resting BNP adjusted odds ratio 2.0, 95% confidence interval 1.3 to 3.0, p = 0.002). In this pilot study, resting BNP was predictive of dobutamine-induced ischemia. Future work is needed to confirm these findings.
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PMID:Usefulness of plasma brain natriuretic peptide levels in predicting dobutamine-induced myocardial ischemia. 1501 72

Since B-type natriuretic peptide (BNP) concentration has been shown by recent studies to be elevated in patients presenting acute coronary syndrome (ACS) even in the absence of overt heart failure, other mechanisms for elevating plasma BNP (p-BNP) concentrations may be suggested to exist. We have studied the correlation between p-BNP level and the extent of myocardial ischemia (EMI) in non-ST elevation (NSTE) ACS and evaluated the BNP level as an objective marker of EMI. In 204 patients with NSTE ACS, we estimated the EMI by the echocardiographic wall motion score index (WMSI) and the coronary angiographic Gensini score. As the positive control group, 44 patients with stable angina were enrolled into the study. We compared their initial p-BNP levels with WMSI and the Gensini score. Additionally, peak troponin-T level was compared with p-BNP level in NSTE myocardial infarction (MI) patients. Using the multiple regression analysis, adjustments for age, left ventricle (LV) wall stress, LV mass amount and ejection fraction (EF) were made. Patients with LVEF < 45% or age > 75 years or underlying diseases that could elevate BNP levels were excluded from the study. P-BNP level was increased in NSTE ACS patients compared with stable angina patients (133.9 +/- 87.4 vs. 12.2 +/- 9.2 pg/ml, p < 0.05). P-BNP levels were found to correlate with WMSI and the Gensini score in unstable angina (r=0.519, p < 0.01; r=0.680, p < 0.01) and NSTEMI (r=0.716, p < 0.01; r=0.684, p < 0.01) patients, respectively. Additionally, p-BNP levels correlated with the peak troponin-T level in patients with NSTEMI (r=0.700, p < 0.01). P-BNP level might be a useful marker in the assessment of EMI.
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PMID:Assessment of extent of myocardial ischemia in patients with non-ST elevation acute coronary syndrome using serum B-type natriuretic peptide level. 1511 97

The natriuretic peptides constitute a family of structurally related peptides that regulate fluid homeostasis, vascular tonus and growth. After the discovery of an endocrine component of the heart almost 25 years ago, the cardiac natriuretic peptides have now been fully accepted as useful markers in diverse aspects of cardiology including as diagnostic, therapeutic and prognostic markers of cardiac disease. In humans, atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are mainly synthesized and secreted by the failing heart, whereas the related C-type natriuretic peptide (CNP) appears to be a local regulatory peptide secreted by the vascular endothelium. Accordingly, CNP is not a cardiac peptide. With the recent implementation of sensitive and specific immunoassays, increased plasma concentrations of proBNP-derived peptides have now been associated with several cardiac conditions, where the major application today seems related to ventricular dysfunction. Recently, focus has also turned to ischemic heart disease, since myocardial hypoxia increases the local BNP gene expression. This review recapitulates the established clinical applications of measuring proBNP-derived peptides in plasma. Furthermore, the evidence of increased cardiac BNP expression in ischemic heart disease will be emphasized. In turn, plasma measurement of proBNP-derived peptides may still hold new possibilities in screening for coronary artery disease.
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PMID:ProBNP-derived peptides in cardiac disease. 1527 15

It is well established that cardiac failure increases cardiac B-type natriuretic peptide (BNP) expression due to myocardial stretching. However, patients with ischemic heart disease also display increased plasma BNP and proBNP concentrations despite preserved cardiac function. In this study, we examined whether acute myocardial hypoxia increases cardiac BNP expression. Surgical reduction of the blood flow to an area of the anterior ventricular wall in pigs reduced the myocardial oxygen tension from 46 +/- 4 to 13 +/- 5 mmHg. The tissue contents of VEGF and BNP mRNA increased 1.8-fold and 3.5-fold, respectively (n=10, P<0.005) in hypoxic compared with normoxic ventricular myocardium after 2.2 +/- 0.2 h; the magnitude of the increase in BNP mRNA expression was positively correlated with that of VEGF in hypoxic myocardium (r=0.66, P<0.05). In support of a hypoxia-induced increase of BNP gene transcription, the content of a premature BNP mRNA was increased in hypoxic myocardium (4.8-fold, P<0.005) and in freshly harvested ventricular myocytes when kept in culture flasks and oxygen-deprived for 3 h (2.2-fold, P=0.002). ProBNP peptide accumulated in the medium of freshly harvested ventricular myocyte cultures but was undetectable in ventricular myocardium, indicating rapid release of the newly synthesized proBNP peptide. Accordingly, the plasma proBNP concentration increased after 2 h of myocardial hypoxia (P=0.028). Cumulatively, the data suggest that acute hypoxia stimulates cardiac BNP expression.
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PMID:Acute myocardial hypoxia increases BNP gene expression. 1557 92

A reduction of coronary flow reserve has been reported in patients with hypertensive heart disease (HHD), which suggests that myocardial ischemia may contribute to the progression to cardiac failure in HHD. Therefore, we evaluated whether fibroblast growth factor (FGF)-2 and/or heparin, which induce angiogenesis, may affect cardiac function in the setting of HHD. We used Dahl salt sensitive (DS) rats as an HHD model. Direct intramyocardial injection of 100 microg of FGF-2 plus 1.28 microg of heparin (n = 6), 100 microg of FGF-2 (n = 6), 1.28 microg of heparin (n = 6) or saline (n = 6) were performed in 9-week-old rats. Echocardiography was performed to evaluate cardiac function at 9, 11, and 13 weeks of age. Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations were measured at 8 and 13 weeks of age. DS rats were killed 4 weeks after myocardial injection (at 13 weeks of age), and myocardial capillary density was assessed by von Willebrand factor staining. Injection of FGF-2 plus heparin significantly decreased left ventricular end-diastolic diameter (P < 0.0001) and left ventricular end-systolic diameter (P < 0.0001), significantly improved the reduction of left ventricular fractional shortening (P = 0.0005), significantly decreased plasma ANP (P < 0.0001) and BNP (P = 0.016) concentrations, and significantly increased myocardial capillary density (P = 0.0002) compared with injection of saline. These findings indicate that intramyocardial injection of FGF-2 plus heparin suppresses the progression of cardiac failure in DS rats. FGF-2 plus heparin administration may be a new therapeutic strategy for the treatment of HHD.
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PMID:Intramyocardial injection of fibroblast growth factor-2 plus heparin suppresses cardiac failure progression in rats with hypertensive heart disease. 1587 12

The natriuretic peptides are hormones released mainly from the cardiac ventricles in response to increased wall tension, and involved in volume homeostasis and cardiovascular remodeling. At today, Atrial Natriuretic Peptide (ANP), Brain Natriuretic Peptide (BNP) and C-type Natriuretic Peptide (CNP) have been identified. BNP is the more utilized, secondary to its major expression of left ventricle function. Recently, it has opened up the potential for the utilization of atrial natriuretic peptides in the everyday clinical practice. The levels of B-type natriuretic peptide are elevated in patients with left ventricular dysfunction and they correlate with both the severity of symptoms and the prognosis. Observational studies have suggested that, when used in conjunction with other clinical information, rapid measurement of B-type natriuretic peptide in the emergency department may be useful in establishing or ruling out the diagnosis of heart failure in patients with acute dyspnea. Furthermore, plasma peptide levels predicted the risk of death and cardiovascular events after adjustment for traditional risk factors. BNP has been studied also in myocardial ischemia: in ST-segment elevation myocardial infarction, BNP rise substantially and rapidly. Elevated levels of BNP can also be detected in patients presenting with non-ST-segment elevation acute coronary syndromes, and even in those with transient myocardial ischemia exercise-induced.
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PMID:[Atrial natriuretic peptides: a new diagnostic tool for the internist]. 1607 61

Chest pain is the most common clinical presentation of acute ischemic heart disease, but only one third of these patients are ultimately found to have an acute coronary syndrome. Initial assessment of the patient presenting with chest pain includes a careful history, physical examination, an initial electrocardiogram (ECG) and measurement of biochemical markers of myocardial injury. The natriuretic peptide system is activated in a broad spectrum of cardiovascular diseases, including acute coronary syndromes and stable coronary disease. A strong relation between plasma levels of B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) obtained in the subacute phase, and long-term, all-cause mortality, as well as the rate of re-admissions for heart failure after myocardial infarction, has been documented. Persistently elevated NT-proBNP levels during the first 72 hours following admission for an acute coronary syndrome have recently been associated with the presence of refractory ischemia and high risk of short-term recurrent ischemic events. Patients with signs of exercise-induced ischemia by dobutamine stress echocardiography have been reported to have higher baseline BNP values. Moreover, BNP and NT-proBNP levels are increased acutely in proportion to the magnitude of the inducible perfusion defect observed during stress testing, suggesting that BNP and NT-proBNP are markers of acute ischemia. Recently, a relationship between circulating levels of BNP and NT-proBNP and long-term all cause mortality in patients with stable coronary artery disease has been documented.
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PMID:Clinical and laboratory diagnostics of cardiovascular disease: focus on natriuretic peptides and cardiac ischemia. 1611 56


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