Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Brain natriuretic peptide (BNP) levels were measured in 100 patients with coronary heart disease (CHD) who underwent myocardial stress thallium-201 single-photon emission computed tomography (30 with stable angina without basal electrocardiographic ischemia and no perfusion defects, 31 with angina with electrocardiographic ischemia and reversible perfusion defects, and 39 with myocardial infarction and irreversible defects) and in 42 controls. BNP levels progressively increased in patients with CHD and were significantly greater in patients with ischemia (p <0.01) and infarction (p <0.001) compared with controls and subjects with angina. BNP concentration was correlated positively (r = 0.923, p <0.001) with perfusion defect extent and inversely (r = -0.690, p <0.001) with the left ventricle ejection fraction (not different in the subjects examined).
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PMID:Usefulness of brain natriuretic peptide levels to discriminate patients with stable angina pectoris without and with electrocardiographic myocardial ischemia and patients with healed myocardial infarction. 1537 88

Excessive excitatory amino acid (EAA) release in cerebral ischemia is a major mechanism responsible for neuronal damage and death. A substantial fraction of ischemic EAA release occurs via volume-regulated anion channels (VRACs). Hydrogen peroxide (H2O2), which is abundantly produced during ischemia and reperfusion, activates a number of protein kinases critical for VRAC functioning and has recently been reported to activate VRACs. In the present study, we explored the effects of H2O2 on volume-dependent EAA release in cultured astrocytes, measured as the release of preloaded D-[3H]aspartate. 100-1,000 microm H2O2 enhanced swelling-induced EAA release by approximately 2.5-3-fold (EC50 approximately 10 microM). The VRAC blockers ATP, phloretin, and 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) potently inhibited both control swelling-induced and the H2O2-potentiated release, suggesting a role for VRACs. The H2O2-induced component of EAA release was attenuated by the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA-AM) and completely eliminated by the calmodulin antagonists trifluoperazine and W-7 and the Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibitor KN-93. Inhibitors of tyrosine kinases, protein kinase C, and the myosin light chain kinase were ineffective in blocking the H2O2 response. H2O2 treatment of swollen astrocytes, but not swelling alone, resulted in CaMKII activation that was inhibited by KN-93, as determined by a phospho-Thr286 CaMKII antibody. These data demonstrate that H2O2 strongly up-regulates astrocytic volume-sensitive EAA release via a CaMKII-dependent mechanism and in this way may potently promote pathological EAA release and brain damage in ischemia.
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PMID:Hydrogen peroxide potentiates volume-sensitive excitatory amino acid release via a mechanism involving Ca2+/calmodulin-dependent protein kinase II. 1556 71

Circulating B-type natriuretic peptide (BNP) is a strong predictor of survival in patients with acute coronary syndromes and in patients with congestive heart failure. Whether circulating BNP levels are predictive of long-term survival in patients with angiographically documented, clinically stable coronary artery disease is unknown. We studied 186 patients with stable angina pectoris and angiographic evidence of significant coronary artery disease. Patients with a recent myocardial infarction, electrocardiographic evidence of ongoing ischemia, anginal pain at rest, or symptomatic congestive heart failure were excluded from the study. During a follow-up of 7.4 years, 23 patients died. By Cox proportional-hazards regression, patient age (p = 0.031), pathologic Q waves on the electrocardiogram (p = 0.037), left ventricular ejection fraction (p = 0.016), and plasma BNP (p = 0.008) were significantly associated with long-term survival. In a stepwise forward multivariate model, BNP (p = 0.005) provided prognostic information above and beyond conventional risk markers. In patients with clinically stable, angiographically documented coronary artery disease, plasma BNP levels are independently related to long-term survival.
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PMID:B-type natriuretic peptide and long-term survival in patients with stable coronary artery disease. 1561 89

Reactive oxygen species (ROS) cause damage to the structure and function of tissues. Therefore tissues have systems that eliminate ROS. Bilirubin is one antioxidant that reacts with ROS to produce oxidative metabolites. Biopyrrins are one of the metabolites, the level of which in urine reflects oxidative stress. They are measured by non-competitive inhibition ELISA that employs anti-bilirubin antibody (24G7) and the results are corrected for the urinary concentration of cereatinine. Some reports suggested that psychological stress increased oxidative stress markers. Urinary biopyrrins were also elevated by speech stress, and the subjective stress score recorded by the speakers correlated with the level. The result suggests that bilirubin might eliminate ROS generated by psychological stress. From the beginning of the study of biopyrrins, their urinary level has been known to be increased by surgical stress. Furthermore, it was significantly higher in a major operation patient group than in a minor one, and correlated with operation duration. Sepsis increased the level in surgical patients. Ischemia-reperfusion elevates ROS and, as a result, biopyrrin production. An increase in urinary biopyrrins was observed in a coronary spastic angina group after a spasm provocation test, and the level in myocardial infarction patients with NYHA (New York Heart Association) classification became higher. Correlation between urinary biopyrrins and plasma B-type natriuretic peptide (BNP) was also reported. Research that determines the structures of biopyrrins and their clinical application are in progress.
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PMID:[Oxidative stress related diseases and biopyrrins]. 1579 50

It has recently been proposed that endothelin-1 (ET-1) is an important activator of natriuretic peptide [atrial natriuretic peptide (ANP) and the brain natriuretic peptide (BNP)] release in the heart and may mediate ANP and BNP deliberation to myocardial stretch and ischemia. The close inter-relationship between ET-1 and natriuretic peptide release was indicated mainly by the results of in vitro studies. In vivo, the local alterations of ANP and BNP levels in the myocardial interstitium can be well characterized by the changes of their pericardial fluid concentrations. The effect of the intrapericardially administered ET-1 on natriuretic peptide concentrations was studied on the in situ dog heart (n = 8). Control and three consecutive infusate samples were removed from the pericardial sac following ET-1 administration (150 pmol/kg) and parallel peripheral blood samples were taken to determine the ANP and BNP concentrations (enzyme-linked immunosorbent assay). Standard hemodynamic parameters were recorded continuously. In our results the intrapericardial ET-1 increased pericardial ANP but not BNP concentrations significantly (control versus ANPmax, 37 +/- 5 ng/mL versus 94 +/- 12 ng/mL; P < 0.02). ET-1 elicited significant ST elevations without changes of the hemodynamic values and the natriuretic peptide levels in the arterial plasma samples. In conclusion, intrapericardial ET-1 effectively stimulated the myocardial ANP release, which was reflected as elevation in the pericardial ANP level. The results also support the hypothesis that important regulatory mechanisms might be activated from the pericardium.
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PMID:Effects of intrapericardially administered endothelin-1 on pericardial natriuretic peptide concentrations of the in situ dog heart. 1583 87

Chronic dyspnea is defined as dyspnea lasting more than one month. In approximately two thirds of patients presenting with dyspnea, the underlying cause is cardiopulmonary disease. Establishing an accurate diagnosis is essential because treatment differs depending on the underlying condition. Asthma, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, cardiac ischemia, interstitial lung disease, and psychogenic causes account for 85 percent of patients with this principal symptom. The history and physical examination should guide selection of initial diagnostic tests such as electrocardiogram, chest radiograph, pulse oximetry, spirometry, complete blood count, and metabolic panel. If these are inconclusive, additional testing is indicated. Formal pulmonary function testing may be needed to establish a diagnosis of asthma, chronic obstructive pulmonary disease, or interstitial lung disease. High-resolution computed tomography is particularly useful for diagnosing interstitial lung disease, idiopathic pulmonary fibrosis, bronchiectasis, or pulmonary embolism. Echocardiography and brain natriuretic peptide levels help establish a diagnosis of congestive heart failure. If the diagnosis remains unclear, additional tests may be required. These include ventilation perfusion scans, Holter monitoring, cardiac catheterization, esophageal pH monitoring, lung biopsy, and cardiopulmonary exercise testing.
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PMID:Evaluation of chronic dyspnea. 1586 93

We studied the relationship between brain natriuretic peptide (BNP) levels and viable myocardium and ischemic myocardium, regional scar and regional contractile function. Fifty-nine patients underwent dobutamine echocardiography and magnetic resonance imaging and resting BNP levels were determined. By magnetic resonance imaging, total extent of dysfunctional myocardium correlated strongest with BNP (r = 0.60, p < 0.0001). The extent of scar, viability and ischemia also correlated. At dobutamine echocardiography, a composite of dysfunctional and ischemic myocardium was the strongest correlate of BNP (r = 0.48, p < 0.0001), with less strong correlations by global parameters. The extent of dysfunctional myocardium, rather than its nature determines BNP levels.
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PMID:Relationship of extent and nature of dysfunctional myocardium to brain natriuretic peptide in patients with ischemic left ventricular dysfunction. 1601 44

Cardiac secretion of B-type natriuretic peptide (BNP) Increases with the progression of heart failure (HF), and plasma measurement of BNP has emerged recently as a useful, cost-effective biomarker for the diagnosis and prognosis of HF. The diagnostic utility of BNP is complemented by its therapeutic use in decompensated HF. Although clinical use of BNP as a biomarker in HF is Increasing, the specificity of BNP for HF is not robust, suggesting that other mechanisms beyond simple ventricular stretch stimulate BNP release. Several studies have shown that BNP levels Increase in other cardiovascular disease states including ischemia, arrhythmias, fibrosis, cardiac hypertrophy, and coronary endothelial dysfunction. Furthermore, 2 important studies revealed recently that moderate elevations In BNP level, well below the HF range, have prognostic value for future cardiovascular events. Specifically, BNP levels greater than 20 pg/mL were associated with significantly Increased risk of HF and atrial fibrillation. These observations increase speculation that elevated BNP levels represent a final common pathway for many cardiovascular pathologic states and that BNP can be used as a biomarker for non-HF mechanisms, preclinical disease, and other pathologic states of myocardial disease.
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PMID:B-type natriuretic peptide as a biomarker beyond heart failure: speculations and opportunities. 2213 32

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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