natriuretic-peptide--brain and Necrosis
natriuretic-peptide--brain has been researched along with Necrosis* in 32 studies
Reviews
6 review(s) available for natriuretic-peptide--brain and Necrosis
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Bench-to-bedside review: the value of cardiac biomarkers in the intensive care patient.
The use of cardiac biomarkers in the intensive care setting is gaining increasing popularity. There are several reasons for this increase: there is now the facility for point-of-care biomarker measurement providing a rapid diagnosis; biomarkers can be used as prognostic tools; biomarkers can be used to guide therapy; and, compared with other methods such as echocardiography, the assays are easier and much more affordable. Two important characteristics of the ideal biomarker are disease specificity and a linear relationship between the serum concentration and disease severity. These characteristics are not present, however, in the majority of biomarkers for cardiac dysfunction currently available. Those clinically useful cardiac biomarkers, which naturally received the most attention, such as troponins and B-type natriuretic peptide, are not as specific as was originally thought. In the intensive care setting, it is important for the user to understand the degree of specificity of these biomarkers and that the interpretation of the results should always be guided by other clinical information. The present review summarizes the available biomarkers for different cardiac conditions. Potential biomarkers under evaluation are also briefly discussed. Topics: Biomarkers; CA-125 Antigen; Cardiovascular Diseases; CD40 Ligand; Choline; Creatine Kinase, MB Form; Fatty Acid Binding Protein 3; Fatty Acid-Binding Proteins; Humans; Intensive Care Units; Interleukins; Myocardium; Natriuretic Peptide, Brain; Necrosis; Peroxidase; Point-of-Care Systems; Sepsis; Serum Albumin; Troponin; Urocortins | 2008 |
The role of existing and novel cardiac biomarkers for cardioprotection.
Cardioprotection is an all-encompassing term for physico-biochemical or therapeutic interventions which slow or ameliorate the progression of cardiomyocyte necrosis. There are a number of established and novel biomarkers to assess coronary artery disease at initiation, ischemia, necrosis and myocardial dysfunction. Established biomarkers such as creatine kinase-MB, cardiac troponins and natriuretic peptides have been utilized for the assessment of cardioprotection, especially during surgery. Novel markers are currently being investigated for detection and risk assessment in patients with acute coronary syndromes. Ischemia-modified albumin is used for the early detection of cardiac ischemia and could be a potential biomarker for assessing the early cardioprotective effects of damage-limiting interventional measures. Topics: Animals; Biological Assay; Biomarkers; Creatine Kinase, MB Form; Disease Progression; Humans; Myocardial Infarction; Myocardial Ischemia; Myocytes, Cardiac; Natriuretic Peptide, Brain; Necrosis; Predictive Value of Tests; Reproducibility of Results; Serum Albumin; Treatment Outcome; Troponin I; Troponin T; Ventricular Dysfunction | 2007 |
Using biomarkers to assess risk and consider treatment strategies in non-ST-segment elevation acute coronary syndromes.
Since the first biomarker of myocardial necrosis was described in 1954, cardiac-specific biomarkers have been increasingly identified. This, coupled with dramatic evolution in assay technology and resultant highly sensitive assays, has rendered a remarkable transformation in the medical use of biomarkers. Initially used to aid in diagnosis of myocardial infarction, newer biomarkers of inflammation, plaque instability, and ischemia may complement biomarkers of necrosis by providing tools to diagnose impending myocardial necrosis before irreversible damage occurs, and offering additional information for risk stratification. Importantly, biomarkers of different processes may be combined to enhance risk stratification above that of any single marker. Topics: Angina, Unstable; Biomarkers; C-Reactive Protein; CD40 Ligand; Humans; Inflammation; Interleukins; Myocardial Infarction; Myocardial Ischemia; Myoglobin; Natriuretic Peptide, Brain; Necrosis; Peroxidase; Pregnancy-Associated Plasma Protein-A; Risk Assessment; Troponin | 2005 |
Pathophysiology, prognostic significance and clinical utility of B-type natriuretic peptide in acute coronary syndromes.
The natriuretic hormones are a family of vasoactive peptides that can be measured circulating in the blood. Because they serve as markers of hemodynamic stress, the major focus of the use of natriuretic peptide levels [predominantly B-type natriuretic peptide (BNP) and N-terminal (NT)-pro-BNP] has been as an aid to the clinical diagnosis and management of congestive heart failure (CHF). Recently, however, the measurement of natriuretic peptides in the acute coronary syndromes (ACS) has been shown to provide information complementary to traditional biomarkers (of necrosis) such as cardiac troponins and creatine kinase (CK). Studies in several types of acute coronary syndromes [ST-segment elevation myocardial infarction (STEMI), non-ST elevation MI (NSTEMI) and unstable angina (UA)] have shown that elevated levels of natriuretic peptides are independently associated with adverse outcomes, particularly mortality. Additional information is obtained from the use natriuretic peptides in combination with other markers of risk including biomarkers of necrosis and inflammation. This review will summarize the scientific rationale and clinical evidence supporting measurement of natriuretic peptides for risk stratification in acute coronary syndromes. Future research is needed to identify therapies of particular benefit for patients with ACS and natriuretic peptide elevation. Topics: Acute Disease; Angina, Unstable; Biomarkers; Coronary Disease; Heart Failure; Humans; Inflammation; Myocardial Infarction; Natriuretic Peptide, Brain; Necrosis; Prognosis; Risk Assessment | 2004 |
Combining natriuretic peptides and necrosis markers in determining prognosis in heart failure.
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. Topics: Biomarkers; Heart Failure; Humans; Natriuretic Peptide, Brain; Necrosis; Prevalence; Prognosis; Troponin; United States; Ventricular Dysfunction, Left | 2003 |
Combining natriuretic peptides and necrosis markers in the assessment of acute coronary syndromes.
Management of patients with acute coronary syndromes (ACS) is becoming more complex as the array of treatment options available to patients and physicians continues to expand. Cardiac biomarkers play an important role in risk stratification in ACS, and results of cardiac biomarker tests can be used to help guide choices between alternative therapies. In addition to biomarkers of myocyte necrosis, markers of neurohormonal activation, such as B-type natriuretic peptide (BNP), provide important prognostic information in ACS. In the future, multimarker strategies that incorporate panels of cardiac biomarkers are likely to be used for risk stratification and for pathophysiology-guided treatment in patients with ACS. Topics: Acute Disease; Biomarkers; C-Reactive Protein; Coronary Disease; Creatine Kinase; Creatine Kinase, MB Form; Humans; Isoenzymes; Myocardium; Natriuretic Peptide, Brain; Necrosis; Nerve Tissue Proteins; Peptide Fragments; Syndrome; Troponin | 2003 |
Trials
2 trial(s) available for natriuretic-peptide--brain and Necrosis
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Baseline NT-proBNP and biomarkers of inflammation and necrosis in patients with ST-segment elevation myocardial infarction: insights from the APEX-AMI trial.
Coronary plaque rupture is associated with a systemic inflammatory response. The relationship between baseline N-terminal pro B-type natriuretic peptide (NT-proBNP), a prognostic marker in patients with acute coronary syndromes, and systemic inflammatory mediators in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) is not well described. Of 5,745 STEMI patients treated with primary PCI in the APEX-AMI trial, we evaluated the relationship between baseline NT-proBNP levels and baseline levels of inflammatory markers and markers of myonecrosis in a subset of 772 who were enrolled in a biomarker substudy. Spearman correlations (r (s)) were calculated between baseline NT-proBNP levels and a panel of ten systemic inflammatory biomarkers. Interleukin (IL)-6, a pro-inflammatory cytokine, was significantly positively correlated with NT-proBNP (r (s) = 0.317, P < 0.001). In a sensitivity analysis excluding all heart failure patients, the correlation between baseline IL-6 and NT-proBNP remained significant (n = 651, r (s) = 0.296, P < 0.001). A positive association was also observed with high sensitivity C-reactive protein (r (s) = 0.377, P < 0.001) and there was a weak negative correlation with the anti-inflammatory cytokine IL-10 (r (s) = -0.109, P = 0.003). No other significant correlations were observed among the other testes inflammatory cytokines and chemokines. In STEMI patients undergoing primary PCI, the pro-inflammatory cytokine IL-6 was modestly correlated with baseline NT-proBNP levels. This relationship remained significant in patients without heart failure. This finding is consistent with pre-clinical and clinical research suggesting that systemic inflammation may influence NT-proBNP expression independently of myocardial stretch. Topics: Aged; Angioplasty, Balloon, Coronary; Biomarkers; Double-Blind Method; Female; Gene Expression Regulation; Humans; Inflammation; Interleukin-10; Interleukin-6; Male; Middle Aged; Myocardial Infarction; Myocardium; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments | 2012 |
Desflurane preconditioning in coronary artery bypass graft surgery: a double-blinded, randomised and placebo-controlled study.
Recent clinical and experimental data indicate that volatile anaesthetics may precondition myocardium against ischaemia and infarction. The present clinical trial was designed to verify the cardioprotective effects of desflurane in patients undergoing elective coronary artery bypass surgery. It was hypothesized that desflurane preconditioning would decrease postoperative release of troponin I and brain natriuretic peptide (NT-proBNP). Besides, we have hypothesized that desflurane preconditioning would preserve the myocardium from the dysfunction following cardioplegic arrest.. Twenty-eight patients were randomly divided into two groups: Control group (14 patients) and Desflurane group (14 patients). In Desflurane group (DS) patients, preconditioning was elicited after the onset of cardiopulmonary bypass via a 5-min exposure to desflurane (2.5 minimum alveolar concentration), followed by a 10-min washout before aortic cross-clamping and cardioplegic arrest. The control group (C) patients underwent an equivalent period (15 min) of pre-arrest desflurane-free bypass. Haemodynamic measurements were obtained at six different times. The biochemistry markers of cellular damage and myocardial dysfunction (troponin I, NT-proBNP) were determined. Left ventricular (LV) function was assessed using tissue Doppler imaging (TDI) of mitral annulus. Two-factor repeated-measures analysis of variance was used to evaluate differences over time between groups for all parameters determined in plasma samples and for all TDI-derived variables.. After surgery, both the troponin I values (2.04+/-1.09 ng/ml vs 1.44+/-0.77 ng/ml, p<0.01 after 24h and 1.62+/-0.96 ng/ml vs 1.00+/-0.24 ng/ml, p<0.01 after 72 h respectively) and those of the NT-proBNP (2187+/-282.9 ng/l vs 885.4+/-117.35 ng/l, p<0.01 after 24h and 3097.9+/-226.2 vs 1393.6+/-312.07 ng/l, p<0.01 after 72 h respectively) were less in the desflurane-treated patients. The values of TDI of mitral annulus were constantly better in desflurane-treated patients.. We can conclude that the use of desflurane in these patients provides a pharmacological preconditioning so as to reduce myocardial necrosis and improve the cardiac performance in the postoperative period. Topics: Anesthetics, Inhalation; Cardiotonic Agents; Coronary Artery Bypass; Coronary Artery Disease; Desflurane; Double-Blind Method; Echocardiography, Doppler; Female; Heart; Humans; Ischemic Preconditioning, Myocardial; Isoflurane; Male; Middle Aged; Myocardium; Natriuretic Agents; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Troponin I; Ventricular Function, Left | 2007 |
Other Studies
24 other study(ies) available for natriuretic-peptide--brain and Necrosis
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Impact of ultra-marathon and marathon on biomarkers of myocyte necrosis and cardiac congestion: a prospective observational study.
An elevation of cardiac biomarkers is observed after intense or long-lasting physical activity. However, a recent meta-analysis has suggested that there might be an inverse relationship between duration of exercise and degree of biomarker elevation. The objective of this observational study was to investigate the impact of ultra-marathon (UM) vs. marathon (M) on biomarkers of myocyte necrosis and hemodynamic stress/congestion.. Well-trained endurance athletes were recruited to participate in a 130-km UM and a M run. Troponin I (TnI), creatine kinase (CK), N-terminal pro-brain natriuretic peptide (NT-proBNP), mid-regional pro-adrenomedullin (MR-proADM), and copeptin were measured after both events, respectively.. Fifteen athletes (14 males, one female) were included. There was no difference in exercise intensity according to the Borg scale (UM 16 [IQR 15-17], M 16 [IQR 14-17]; p = 0.424). Biomarkers of myocyte necrosis both differed significantly with higher levels of TnI (UM 0.056 ng/L [IQR 0.022-0.104), M 0.028 ng/L [IQR 0.022-0.049]; p = 0.016) and CK (UM 6992 U/l [IQR 2886-23038], M 425 U/l [IQR 327-681]; p = 0.001) after UM compared to M. Also, NT-proBNP (UM 723 ng/L [IQR 378-1152], M 132 ng/L [IQR 64-198]; p = 0.001) and MR-proADM (UM 1.012 nmol/L [IQR 0.753-0.975], M 0.877 nmol/L [IQR 0.550-0.985]; p = 0.023) as markers of myocardial congestion were significantly higher after UM. There was a tendency for elevated copeptin levels after M, but did not reach statistical significance (p = 0.078).. Ultra-marathon is associated with higher levels of biomarkers of myocyte necrosis and cardiac congestion compared to marathon, highlighting the impact of exercise duration on the cardiovascular system. Topics: Adult; Athletes; Biomarkers; Female; Humans; Male; Marathon Running; Middle Aged; Myocytes, Cardiac; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Prospective Studies; Protein Precursors; Troponin I; Troponin T; Young Adult | 2020 |
The Endogenous Lusitropic and Chronotropic Agent, B-Type Natriuretic Peptide, Limits Cardiac Troponin Release in Cancer Patients with an Early Impairment of Myocardial Relaxation Induced by Anthracyclines.
We have reported that cancer patients treated with anthracycline-based or nonanthracycline chemotherapy developed an early impairment of myocardial relaxation at echocardiography or persistent elevations of the cardiac hormone B-type natriuretic peptide (BNP). Post-hoc pharmacologic analyses showed that BNP elevations were induced by impaired relaxation and caused positive lusitropic effects that maintained normal relaxation. High BNP levels and impaired relaxation were therefore characterized as mutually exclusive manifestations of diastolic dysfunction, but high BNP levels resulted in positive chronotropism and inappropriate tachycardia. Some patients developed increased circulating levels of cardiac troponin I isoform (cTnI), a marker of cardiomyocyte necrosis. Here we have characterized whether cTnI elevations correlated with diastolic dysfunction that manifested as impaired relaxation or a high level of BNP. The effects of high BNP levels on cTnI elevations were also characterized. We show that impaired relaxation or high BNP levels were significantly more frequent in patients with cTnI elevations. High BNP levels diminished the plasma peak and area under the curve of cTnI, but this result was accompanied by inappropriate tachycardia. cTnI elevations occurred only in patients treated with anthracyclines; moreover, the association of impaired relaxation or high BNP levels with cTnI elevations was significantly more frequent in doxorubicin-treated patients compared with patients treated with its analog, epirubicin. These findings describe cause-and-effect relations between impaired relaxation and cardiomyocyte necrosis, illuminate the role of anthracycline analogs, denote that the beneficial effects of BNP in relieving impaired relaxation and cardiomyocyte necrosis are counterbalanced by inappropriate tachycardia. Patients showing troponin elevations and impaired relaxation or high BNP levels should be treated with lusitropic drugs that lack a positive chronotropism. Topics: Adult; Anthracyclines; Biomarkers; Doxorubicin; Epirubicin; Female; Heart; Humans; Male; Middle Aged; Myocardium; Natriuretic Peptide, Brain; Necrosis; Neoplasms; Pilot Projects; Troponin I | 2018 |
Concentrations of highly sensitive cardiac troponin-I predict poor cardiovascular outcomes and adverse remodeling in chronic heart failure.
Highly sensitive troponin (hsTn) assays may predict cardiovascular (CV) events and left ventricular (LV) remodeling in patients with heart failure (HF). In this study, 99 subjects with LV systolic dysfunction (LVSD) were followed 10 ± 3 months with serial measurement of hsTnI by a novel method. hsTnI was detectable in all subjects and was above the 99th percentile of a normal population in 56.7 %. Supramedian baseline hsTnI concentration was associated with higher-risk clinical features and shorter time-to-first event (p = 0.008). Across serial measurements, more time spent ≤ 10.9 pg/mL was associated with a lower CV event rate after adjustment (odds ratio (OR) = 0.81; p = 0.008); rising hsTnI also predicted progressive LV remodeling. In conclusion, hsTnI detected significant myocardial necrosis in a majority of patients with chronic HF due to LVSD and when measured serially, provided independent risk information for poor CV outcomes and deleterious LV remodeling. Topics: Aged; Aged, 80 and over; Biomarkers; Chi-Square Distribution; Chronic Disease; Disease Progression; Female; Heart Failure; Humans; Kaplan-Meier Estimate; Male; Middle Aged; Multivariate Analysis; Myocardium; Natriuretic Peptide, Brain; Necrosis; Odds Ratio; Peptide Fragments; Phenotype; Predictive Value of Tests; Prognosis; Proportional Hazards Models; Randomized Controlled Trials as Topic; Retrospective Studies; Risk Factors; Systole; Time Factors; Troponin I; Ventricular Dysfunction, Left; Ventricular Function, Left; Ventricular Remodeling | 2015 |
Sensitive cardiac troponins and N-terminal pro-B-type natriuretic peptide in stable coronary artery disease: correlation with left ventricular function as assessed by myocardial strain.
N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponins (cTns) measured with sensitive assays provide strong prognostic information in patients with stable coronary artery disease. However, the relationship between these biomarkers and myocardial contractile function, as well as infarct size, in this patient group, remains to be defined. The study population consisted of 160 patients referred to a follow-up echocardiography scheduled 1 year after coronary revascularization. Concentrations of NT-proBNP, high-sensitive cTnT (hs-cTnT) and sensitive cTnI assays were assessed. Left ventricular function was measured as global peak systolic longitudinal strain by speckle tracking echocardiography and infarct size was assessed by late-enhancement MRI. NT-proBNP and sensitive cTnI levels were significantly associated with left ventricular function by peak systolic strain (R-values 0.243 and 0.228, p = 0.002 and 0.004) as well as infarct size (R-values 0.343 and 0.366, p = 0.014 and p = 0.008). In contrast, hs-cTnT did not correlate with left ventricular function (R = 0.095, p = 0.231) and only marginally with infarct size (R = 0.237, p = 0.094). NT-proBNP and sensitive cTnI levels correlate with left ventricular function and infarct size in patients with stable coronary artery disease after revascularization. As opposed to hs-cTnT, NT-proBNP and cTnI seem to be indicators of incipient myocardial dysfunction and the extent of myocardial necrosis. Topics: Aged; Biomarkers; Biomechanical Phenomena; Coronary Angiography; Coronary Artery Disease; Echocardiography; Female; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Myocardial Revascularization; Myocardium; Natriuretic Peptide, Brain; Necrosis; Norway; Peptide Fragments; Predictive Value of Tests; Prospective Studies; Stress, Mechanical; Time Factors; Treatment Outcome; Troponin I; Troponin T; Ventricular Function, Left; Ventricular Remodeling | 2015 |
Time course changes of cystatin C and inflammatory and biochemical markers in non-ST-elevation acute coronary syndromes.
Serum cystatin C (Cys-C), a good marker of renal function, predicts prognosis in non-ST-elevation acute coronary syndromes (NSTE-ACS). However, no data are available on the time course of Cys-C values after discharge. In this study, Cys-C was measured during admission (ACS sample) and 6 weeks after discharge, and was correlated with troponin (c-TNT), high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL-6) and the N-terminal portion of the pro-brain natriuretic peptide (proBNP) peptide (NT-proBNP) in a highly selected homogeneous group of NSTE-ACS patients.. In this prospective, multicentre study, patients with a first NSTE-ACS, single-vessel disease and successful percutaneous coronary interventions (PCIs) had their sera collected, aliquoted and stored at the enrolling site and then shipped for analysis to the clinical chemistry core laboratory.. Cys-C values slightly, but significantly, increased from the ACS samples to the 6-week samples. In contrast, hsCRP, NT-proBNP and IL-6 values significantly decreased from the ACS to the 6-week sample. Patients with elevated c-TNT levels had higher hsCRP, NT-proBNP and IL-6 values than patients with normal c-TNT levels in the ACS sample, whereas Cys-C levels were similar in patients with and without elevated c-TNT. Cys-C was highly correlated with estimated glomerular filtration rate in both the ACS and 6-week samples.. In contrast to inflammatory and biochemical stress markers, Cys-C is not affected by the occurrence of myocardial necrosis or by acute left-ventricular impairment, being a reliable marker of renal function during NSTE-ACS. Topics: Acute Coronary Syndrome; Biomarkers; C-Reactive Protein; Cystatin C; Female; Humans; Inflammation Mediators; Interleukin-6; Italy; Male; Middle Aged; Myocardial Infarction; Myocardium; Natriuretic Peptide, Brain; Necrosis; Patient Admission; Patient Discharge; Peptide Fragments; Percutaneous Coronary Intervention; Prospective Studies; Risk Factors; Time Factors; Treatment Outcome; Troponin; Ventricular Function, Left | 2014 |
NT-proBNP for prognostic and diagnostic evaluation in patients with acute coronary syndromes.
N terminal-proB-type natriuretic peptide (NT-proBNP) is synthesised and secreted from the ventricular myocardium. This marker is known to be elevated in patients with acute coronary syndromes (ACS). We evaluated NT-proBNP asa significant diagnostic marker and an important independent predictor of short-term mortality (one month) in patients with ACS.. NT-proBNP and cardiac troponin I (cTI) were assessed in 134 consecutive patients (median age 66 years, 73% male)hospitalised for ACS in a cardiological university department. The patients were classified into ST-elevation ACS (STE-ACS, n = 74) and non-ST-elevation ACS (NSTE-ACS, n = 60) groups based on the ECG findings on admission. Patients with Killip class ≥ II were excluded.. The serum level of NT-proBNP on admission was significantly higher (p < 0.0005), while there was no difference in cTI serum level in the NSTE-ACS patients compared to STE-ACS patients. There was a significant positive correlation between NT-proBNP and cTI in the NSTE-ACS (r = 0.338, p = 0.008) and STE-ACS (r = 0.441, p < 0.0005) patients. There was a significant difference in NT-proBNP (p < 0.0005) and cTI (p < 0.0005) serum level between ACS patients who died within 30 days or who survived after one month. The increased NT-proBNP level is the strongest predictor of mortality in ACS patients, also NT-proBNP cut-point level of 1,490 pg/mL is a significant independent predictor of mortality.. We demonstrated the differences and the correlation in the secretion of NT-proBNP and cTI in patients with STE-ACS vs. NSTE-ACS. Our results provide evidence that NT-proBNP is a significant diagnostic marker and an important independent predictor of short-term mortality in patients with ACS. Topics: Acute Coronary Syndrome; Aged; Biomarkers; Coronary Angiography; Female; Humans; Logistic Models; Male; Myocardial Ischemia; Myocardium; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Percutaneous Coronary Intervention; Prognosis; Prospective Studies; ROC Curve; Stents; Survival Rate; Troponin I | 2013 |
Growth differentiation factor 15, ST2, high-sensitivity troponin T, and N-terminal pro brain natriuretic peptide in heart failure with preserved vs. reduced ejection fraction.
Growth differentiation factor 15 (GDF15), ST2, high-sensitivity troponin T (hsTnT), and N-terminal pro brain natriuretic peptide (NT-proBNP) are biomarkers of distinct mechanisms that may contribute to the pathophysiology of heart failure (HF) [inflammation (GDF15); ventricular remodelling (ST2); myonecrosis (hsTnT); and wall stress (NT-proBNP)].. We compared circulating levels of GDF15, ST2, hsTnT, and NT-proBNP, as well as their combinations, in compensated patients with clinical HF with reduced ejection fraction (HFREF) (n = 51), HF with preserved ejection fraction (HFPEF) (n= 50), and community-based controls (n = 50). Compared with controls, patients with HFPEF and HFREF had higher median levels of GDF15 (540 pg/mL vs. 2529 and 2672 pg/mL, respectively), hsTnT (3.7 pg/mL vs. 23.7 and 35.6 pg/mL), and NT-proBNP (69 pg/mL vs. 942 and 2562 pg/mL), but not ST2 (27.6 ng/mL vs. 31.5 and 35.3 ng/mL), adjusting for clinical covariates. In receiver operating characteristic curve analyses, NT-proBNP distinguished HFREF from controls with an area under the curve (AUC) of 0.987 (P < 0.001); GDF15 distinguished HFPEF from controls with an AUC of 0.936 (P < 0.001); and the combination of NT-proBNP and GDF15 distinguished HFPEF from controls with an AUC of 0.956 (P < 0.001). NT-proBNP and hsTnT levels were higher in HFREF than in HFPEF (adjusted P < 0.04). The NT-proBNP:GDF15 ratio distinguished between HFPEF and HFREF with the largest AUC (0.709; P < 0.001).. Our study provides comparative data on physiologically distinct circulating biomarkers in HFPEF, HFREF, and controls from the same community. These data suggest a prominent role for myocardial injury (hsTnT) with increased wall stress (NT-proBNP) in HFREF, and systemic inflammation (GDF15) in HFPEF. Topics: Area Under Curve; Biomarkers; Case-Control Studies; Echocardiography, Doppler; Electrocardiography; Female; Growth Differentiation Factor 15; Heart Failure; Humans; Inflammation; Interleukin-1 Receptor-Like 1 Protein; Male; Middle Aged; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Prospective Studies; Receptors, Cell Surface; ROC Curve; Singapore; Stroke Volume; Troponin T; Ventricular Remodeling | 2012 |
High-sensitive troponin, B-type natriuretic peptide and coronary angiogram findings in patients with non ST-segment elevation acute coronary syndrome.
Topics: Acute Coronary Syndrome; Aged; Aged, 80 and over; Angina, Unstable; Biomarkers; Cohort Studies; Coronary Angiography; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Necrosis; Troponin | 2011 |
NT-proBNP levels in patients with non-ST-segment elevation acute coronary syndrome.
Non-ST-segment elevation acute coronary syndrome is associated with elevation of brain natriuretic peptide and markers of myocardial necrosis, although its relationship with the TIMI score and left ventricular function are largely unknown.. To evaluate the correlation between plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) and markers of myocardial necrosis [creatine phosphokinase muscle-brain fraction (CK-MB) and troponin I], TIMI risk score and left ventricular ejection fraction in patients with non-ST-segment elevation acute coronary syndrome.. Eighty-seven patients with non-ST-segment elevation acute coronary syndrome were divided into two groups: 37 (42.5%) with unstable angina and 50 (57.5%) with non-ST-segment elevation myocardial infarction.. Left ventricular ejection fraction more than 40% was found in 86.2% of the total sample. Serum levels of NT-proBNP was higher in patients with non-ST elevation myocardial infarction than in those with unstable angina (p<0.001). Increased levels of NT-proBNP were associated with increases in troponin I (rs=0.425, p<0.001), peak CK-MB (rs=0.458, p<0.001) and low left ventricular ejection fraction (rs=-0.345, p=0.002); no correlation was found with the TIMI risk score (rs=0.082, p=0.44). Multivariate analysis revealed that left ventricular ejection fraction and troponin I levels were independently correlated with NT-proBNP levels (p=0.017 and p=0.002, respectively).. Increased levels of NT-proBNP in patients with non-ST-segment elevation acute coronary syndrome are not related exclusively to low left ventricular ejection fraction, but can also be caused by the presence of myocardial ischemia and necrosis. Topics: Acute Coronary Syndrome; Biomarkers; Creatine Kinase, MB Form; Epidemiologic Methods; Female; Humans; Male; Middle Aged; Myocardium; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Risk Assessment; Stroke Volume; Troponin I | 2011 |
Improving long-term risk prediction in patients with acute chest pain: the Global Registry of Acute Coronary Events (GRACE) risk score is enhanced by selected nonnecrosis biomarkers.
The Global Registry of Acute Coronary Events (GRACE) risk score is widely recommended for risk assessment in patients with acute coronary syndrome. However, there is limited knowledge regarding the utility of this score for long-term risk prediction in unselected patients with acute chest pain and whether it might be improved by the integration of nonnecrosis biomarkers.. We calculated the GRACE risk score in 453 chest pain patients and assessed its value for risk assessment together with the additive prognostic information obtained from N-terminal pro-B-type natriuretic peptide, C-reactive protein, growth differentiation factor-15 (GDF-15), and cystatin C.. After a median follow-up of 5.8 years, 92 patients (20.7%) had died. The GRACE risk score was significantly higher in patients who died (median 146 vs 93, P < .001) and provided a c-statistic regarding mortality of 0.78. A significant increase of the c-statistic was achieved only after addition of GDF-15 (c-statistic 0.81, P = .003) and, to a minor extent, after addition of cystatin C (c-statistic 0.81, P = .035). Assessment of the integrated discriminative improvement yielded similar results. N-terminal pro-B-type natriuretic peptide had only limited incremental prognostic value, and C-reactive protein was not predictive for outcome.. The GRACE risk score allows for the prediction of mortality in chest pain patients even after almost 6 years of follow-up. However, its predictive value could be further enhanced by the addition of selected nonnecrosis biomarkers, in particular GDF-15 or cystatin C. Topics: Acute Coronary Syndrome; Aged; Aged, 80 and over; Biomarkers; C-Reactive Protein; Chest Pain; Coronary Care Units; Disease Progression; Electrocardiography; Female; Follow-Up Studies; Growth Differentiation Factor 15; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Prevalence; Prognosis; Protein Precursors; Registries; Retrospective Studies; Risk Assessment; Risk Factors; Salivary Cystatins; Severity of Illness Index; Sweden; Time Factors; Troponin I | 2010 |
Capturing the pathophysiology of acute coronary syndromes with circulating biomarkers.
There have been considerable advances in the evaluation of suspected acute coronary syndromes (ACS): sophistication of the clinical examination, electrocardiography, risk prediction scores, multiple blood biomarkers, and rapid cardiovascular imaging. Integration of information remains a formidable challenge for the physician in the setting of time-sensitive clinical decision making. In addition to conventional panels of biomarkers, there are novel entities that may be able to signal different stages of the acute event, including plaque disruption, atherothrombosis, ischemic damage, tissue hypoxia, and oxidative stress. The natriuretic peptides are normal myocyte products that reflect myocardial tissue response to neurohormonal and mechanical forces that rapidly change during an ACS event. This article summarizes major advancements in the integrative use of multiple blood biomarkers and cardiovascular imaging in the diagnosis, prognosis, and management of ACS. Topics: Acute Coronary Syndrome; Biomarkers; Fibrosis; Humans; Lipids; Myocardium; Natriuretic Peptide, Brain; Necrosis; Oxidative Stress; Predictive Value of Tests; Prognosis | 2010 |
B-type natriuretic peptide release and left ventricular filling pressure assessed by echocardiographic study after subarachnoid hemorrhage: a prospective study in non-cardiac patients.
Serum B-type natriuretic peptide (BNP) is frequently elevated after subarachnoid hemorrhage (SAH), but whether this high BNP level is related to transient elevation of left ventricular filling pressure (LVFP) is unknown. However, in patients with preexistent cardiac pathologies, it is impossible to differentiate between BNP elevation caused by chronic cardiac abnormalities and BNP related to acute neurocardiac injury.. All adult patients with SAH admitted to our intensive care unit were eligible. Patients were excluded for the following reasons: admission >48 hours after aneurysm rupture, pre-existing hypertension, or cardiac disease. Levels of BNP and cardiac troponin Ic were measured daily for 7 days. Echocardiography was performed by a blinded cardiologist on days 1, 2, and 7. Doppler signals from the mitral inflow, tissue Doppler, and the color M-mode-derived flow propagation velocity (FPV) were obtained to assess echo-estimated LVFP.. During a 3-year period, sixty-six consecutive patients with SAH were admitted. Thirty one patients were studied. The BNP level was >100 ng/L in 25 patients (80%) during the first 3 days, with a peak on day 2 (median, 126 ng/L) followed by a gradual decrease (median variation days 1 to 7, 70%). All patients had an ejection fraction >50%. Early transmitral velocity/tissue Doppler mitral annular early diastolic velocity was low: 5.4 (+/- 1.5) on day 1, 5.8 (+/- 1.2) on day 2, and 5.1 (+/- 0.9) on day 7. Early transmitral velocity/FPV was also low: 1.27 (+/- 0.4), 1.25 (+/- 0.3), and 1.1 (+/- 0.2) on days 1, 2, and 7, respectively. Cardiac troponin Ic levels ranged from 0 to 3.67 microg/L and were correlated with BNP (r = 0.63, P < 0.01).. BNP rises gradually over two days and return to normal within a week after SAH. Its release is associated with myocardial necrosis, but is unrelated to elevated LVFP assessed by echocardiography. Topics: Acute Disease; Adult; Cardiomyopathies; Echocardiography, Doppler; Female; Hemodynamics; Humans; Male; Natriuretic Peptide, Brain; Necrosis; Prospective Studies; Subarachnoid Hemorrhage; Troponin I; Ventricular Dysfunction, Left | 2009 |
Relation between N-terminal pro-B-type natriuretic peptide and coronary plaque components in patients with acute coronary syndrome: virtual histology-intravascular ultrasound analysis.
The N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) is a sensitive indicator of hemodynamic stress and its increased level is associated with higher mortality in acute coronary syndrome (ACS) patients. Virtual histology-intravascular ultrasound (VH-IVUS) can provide quantitative information on plaque components.. We measured preprocedural serum NT-pro-BNP levels in 156 ACS patients with preserved left ventricular systolic function and normal serum creatinine. VH-IVUS classified the color-coded tissue into four major components: fibrotic, fibro-fatty, dense calcium, and necrotic core (NC). Thin-cap fibroatheroma (TCFA) was defined as focal, NC-rich (>or=10% of the cross-sectional area) plaques being in contact with the lumen in a plaque burden of at least 40%. We divided the patients into two groups according to the NT-pro-BNP levels [group I: >or=200 pg/ml (n = 58) vs. group II: <200 pg/ml (n = 98)].. The percent areas of NC at the minimum lumen site (19.8+/-13.1% vs. 15.2+/-11.1%, P = 0.027) and at the largest NC site (24.7+/-10.3% vs. 19.2+/-11.4%, P = 0.015) were significantly greater in group I than in group II. Percent NC volume was significantly greater in group I than in group II (15.8+/-8.1% vs. 10.1+/-9.1%, P = 0.008). The total number of TCFAs was 38 in group I and 56 in group II. The presence of at least one TCFA (58 vs. 38%, P = 0.009) and multiple TCFAs (25 vs. 10%, P = 0.005) within culprit lesions were observed more frequently in group I than in group II. The TCFAs were located more in proximal in group I than in group II [the length from coronary ostium to TCFA: 10.8+/-7.6 mm in group I vs. 25.7+/-16.3 mm in group II (P<0.001)]: 85% of TCFAs was located within 20 mm from coronary ostium in group I; conversely only 36% of TCFAs was located within 20 mm from coronary ostium in group II (P<0.001).. VH-IVUS analysis shows that ACS patients with high NT-pro-BNP levels had more vulnerable plaque component (more NC-containing lesions and higher frequency of culprit lesion TCFAs) and had more proximally located TCFAs. Topics: Acute Coronary Syndrome; Aged; Angioplasty, Balloon, Coronary; Biomarkers; Calcinosis; Coronary Angiography; Coronary Artery Disease; Coronary Vessels; Creatinine; Female; Fibrosis; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Predictive Value of Tests; Retrospective Studies; Ultrasonography, Interventional; Up-Regulation; Ventricular Function, Left | 2009 |
Cardiac biomarkers in chronic renal disease.
Cardiac biomarkers have a complex interrelationship with disease pathophysiology in patients with renal dysfunction. The underlying clinical condition results in a direct effect on the normal release and clearance of cardiac troponins and natriuretic peptides. Although initial reports suggested that this might prove a major limitation in the routine clinical use of these markers, a combination of improved assay performance and a better understanding of the underlying biochemistry of these markers in health and disease has clarified the situation. Renal dysfunction does not provide a significant practical limitation to the use of cardiac biomarkers for diagnosis in acute presentation of cardiovascular disease. The direct relationship between cardiac biomarkers and renal dysfunction reflects the high incidence of cardiovascular disease and cardiac death in patients with renal dysfunction and end-stage renal disease. Elevations of the cardiac troponins are prognostic in patients with renal dysfunction and represent global diffuse myocardial injury. Elevations of natriuretic peptides also occur due to abnormalities of ventricular function. In addition, background levels will be affected by fluid and electrolyte abnormalities due to renal dysfunction. This will directly affect vascular volume and fluid distribution altering atrial and ventricular wall tension and hence rates of natriuretic peptide release and production. The challenge is for the renal physician to translate the potential for cardiovascular disease monitoring conferred by these biomarkers into improved patient management. Topics: Atrial Natriuretic Factor; Biomarkers; Humans; Kidney Failure, Chronic; Myocytes, Cardiac; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Troponin I; Troponin T | 2008 |
Natriuretic peptides modify Pseudomonas fluorescens cytotoxicity by regulating cyclic nucleotides and modifying LPS structure.
Nervous tissues express various communication molecules including natriuretic peptides, i.e. Brain Natriuretic Peptide (BNP) and C-type Natriuretic Peptide (CNP). These molecules share structural similarities with cyclic antibacterial peptides. CNP and to a lesser extent BNP can modify the cytotoxicity of the opportunistic pathogen Pseudomonas aeruginosa. The psychrotrophic environmental species Pseudomonas fluorescens also binds to and kills neurons and glial cells, cell types that both produce natriuretic peptides. In the present study, we investigated the sensitivity of Pseudomonas fluorescens to natriuretic peptides and evaluated the distribution and variability of putative natriuretic peptide-dependent sensor systems in the Pseudomonas genus.. Neither BNP nor CNP modified P. fluorescens MF37 growth or cultivability. However, pre-treatment of P. fluorescens MF37 with BNP or CNP provoked a decrease of the apoptotic effect of the bacterium on glial cells and an increase of its necrotic activity. By homology with eukaryotes, where natriuretic peptides act through receptors coupled to cyclases, we observed that cell-permeable stable analogues of cyclic AMP (dbcAMP) and cyclic GMP (8BcGMP) mimicked the effect of BNP and CNP on bacteria. Intra-bacterial concentrations of cAMP and cGMP were measured to study the involvement of bacterial cyclases in the regulation of P. fluorescens cytotoxicity by BNP or CNP. BNP provoked an increase (+49%) of the cAMP concentration in P. fluorescens, and CNP increased the intra-bacterial concentrations of cGMP (+136%). The effect of BNP and CNP on the virulence of P. fluorescens was independent of the potential of the bacteria to bind to glial cells. Conversely, LPS extracted from MF37 pre-treated with dbcAMP showed a higher necrotic activity than the LPS from untreated or 8BcGMP-pre-treated bacteria. Capillary electrophoresis analysis suggests that these different effects of the LPS may be due, at least in part, to variations in the structure of the macromolecule.. These observations support the hypothesis that P. fluorescens responds to natriuretic peptides through a putative sensor system coupled to a cyclase that could interfere with LPS synthesis and thereby modify the overall virulence of the micro-organism. Topics: Animals; Apoptosis; Cells, Cultured; Cyclic AMP; Cyclic GMP; L-Lactate Dehydrogenase; Lipopolysaccharides; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Necrosis; Neuroglia; Nitric Oxide Synthase; Pseudomonas fluorescens; Rats | 2008 |
Severe septic inflammation as a strong stimulus of myocardial NT-pro brain natriuretic peptide release.
Septic shock (SS) has recently been identified as stimulus of N-terminal pro-brain natriuretic peptide (NT-proBNP) release. We tested whether SS mediates NT-proBNP release through cardiomyocyte necrosis. Moreover, the discriminative value of NT-proBNP for the distinction between SS and non-septic shock (NSS) was assessed.. The study included 50 ICU patients with SS (n=25) and NSS (n=25), 40 patients with acute coronary syndrome and elevated troponin-I (ACStrop+) and 16 patients with unstable angina and normal troponin-I (UAtrop-). Eleven subjects without inflammation or cardiac disease served as controls. NT-proBNP levels of coronary patients were measured on admission, those of ICU patients 48 h after onset of shock symptoms.. ACStrop+ (1525 [25th-75th percentile: 790-3820] pg/L) and NSS (687 [254-1552]) patients showed increased NT-proBNP levels above those of UAtrop- patients (107 [43-450], p<0.001) and controls (52 [42-99], p<0.001), but SS patients exhibited still higher levels (11,335 [4716-25,769], p<0.001 vs all others). Among ICU patients with shock symptoms, NT-proBNP discriminated SS and NSS with high sensitivity and specificity (area under ROC curve: 0.946 [95% confidence interval, 0.872-1.019]). NT-proBNP correlated with troponin-I, as marker of cardiomyocyte damage, among ACStrop+ (p<0.001) and SS patients (p=0.013). But, whereas SS patients showed the greatest NT-proBNP values, ACStrop+ patients had higher troponin-I levels (p<0.001), suggesting different mechanisms by which myocardial ischemia and SS mediate NT-proBNP release.. SS is a more potent stimulus of NT-proBNP release than myocardial ischemia. NT-proBNP reliably distinguishes SS from other forms of shock. SS-related NT-proBNP release appears to involve cardiomyocyte damage but not genuine cardiomyocyte necrosis. Topics: Aged; Angina, Unstable; APACHE; Comorbidity; Female; Humans; Male; Middle Aged; Myocardial Infarction; Myocardium; Myocytes, Cardiac; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Prognosis; Shock, Septic; Syndrome | 2007 |
Difference in elevation of N-terminal pro-BNP and conventional cardiac markers between patients with ST elevation vs non-ST elevation acute coronary syndrome.
N-terminal pro-B-type natriuretic peptide (NT-proBNP) is elevated in patients with acute coronary syndrome (ACS), and is a powerful predictor of long-term mortality. Differences in the clinical utility and pathophysiological implication of NT-proBNP and conventional cardiac markers in patients with ST elevation (STE) vs non-STE (NSTE) ACS were investigated in the present study.. Ninety consecutive patients admitted with acute chest pain and a diagnosis of unstable angina or acute myocardial infarction were analyzed. Patients with >or=Killip class II were excluded to focus on the effect of myocardial ischemia on the release of cardiac markers. The markers were measured on admission and analyzed according to the time from onset. Conventional cytosolic marker (creatine kinase-MB) and myofibril marker (troponin T: TnT) were both significantly higher in STE-ACS patients compared with NSTE-ACS patients. Conversely, NT-proBNP was significantly higher in NSTE-ACS patients than STE-ACS especially within 3 h of onset, suggesting a larger ischemic insult despite the smaller extent of myocardial necrosis compared with STE-ACS patients. There was no significant correlation between NT-proBNP level and left ventricular ejection fraction (LVEF) obtained at acute-phase echocardiography in either NSTE-ACS patients (LVEF 57.7+/-11.2%) or STE-ACS patients (LVEF 55.1+/-12.7%). Comparison between NT-proBNP and TnT levels revealed a marked difference of elevations, with significantly augmented elevation of NT-proBNP (p<0.001) in NSTE-ACS patients as compared with prominent elevation of TnT in STE-ACS patients.. NT-proBNP is an early sensitive marker of myocardial ischemia that rises much higher in the earlier phase as compared with conventional markers of myocardial damage, especially in NSTE-ACS patients. Topics: Aged; Angina, Unstable; Biomarkers; Coronary Thrombosis; Creatine Kinase, MB Form; Electrocardiography; Female; Humans; Male; Middle Aged; Myocardial Infarction; Myocardial Ischemia; Myocardium; Natriuretic Peptide, Brain; Necrosis; Peptide Fragments; Syndrome; Tachycardia, Sinus; Troponin T; Ventricular Dysfunction, Left | 2006 |
Changes in production and metabolism of brain natriuretic peptide in rats with myocardial necrosis.
In this study, we employed rat model of acute myocardial necrosis induced by isoproterenol (ISO) to study the possible roles of corin, the protease uniquely distributing in myocardium to convert pro-brain natriuretic peptide (proBNP) to BNP, and neutral endopeptidase (NEP), the major enzyme to degrade BNP, in changing the levels of BNP. In rats with isoproterenol alone, the myocardium necrosis occurred and the cardiac function was inhibited; the BNP contents in plasma and myocardium were upregulated, so did the myocardial corin mRNA level; the NEP activity in plasma and myocardium were downregulated. Omapatrilat (OMA) treatment relieved myocardial lesions and improved cardiac function. In the plasma and myocardium, omapatrilat treatment increased BNP contents, reduced NEP activity; in myocardium, mRNA level of proBNP and corin decreased, but NEP mRNA expression increased. Our study confirmed that omapatrilat treated myocardial necrosis effectively and suggested that increased BNP in rats with myocardial necrosis could depend on increased production and conversion as well as decreased degradation. Topics: Animals; Isoproterenol; Male; Myocardium; Natriuretic Peptide, Brain; Necrosis; Pyridines; Rats; Rats, Sprague-Dawley; Thiazepines | 2005 |
Cardiac response to prolonged strenuous exercise: a physiologic model for stunning myocardium.
Topics: Bicycling; Heart Function Tests; Humans; Myocardial Stunning; Myocardium; Natriuretic Peptide, Brain; Necrosis; Nerve Tissue Proteins; Peptide Fragments; Physical Endurance; Running; Sports; Troponin I; Troponin T | 2005 |
Clinical significance of increased cardiac troponins T and I in participants of ultra-endurance events.
Of 105 asymptomatic finishers of endurance competitive events lasting several hours, increased blood concentrations of cardiac troponins T and I above the 99% upper reference values were found in 24 and 34 subjects, respectively; N-terminal pro-brain natriuretic peptide was also significantly increased. Within 3 months after the events, 21 troponin-positive participants underwent an extensive cardiac examination, which in all but 1 (critical coronary heart disease) revealed no signs of persistent cardiac damage. Topics: Adult; Bicycling; Female; Heart Function Tests; Humans; Male; Middle Aged; Myocardium; Natriuretic Peptide, Brain; Necrosis; Nerve Tissue Proteins; Peptide Fragments; Physical Endurance; Running; Sports; Troponin I; Troponin T | 2004 |
Brain natriuretic peptide and other cardiac markers in predicting left ventricular remodeling in patients with the first myocardial infarction.
Left ventricular remodeling is a complex pathologic process of progressive dilatation, leading to dysfunction and heart failure in patients with acute myocardial infarction. The aim of our study was to determine and evaluate biochemical markers, reflecting cardiac remodeling process in the patients with the first myocardial infarction and to compare those markers with clinical characteristics of left ventricular remodeling.. Concentrations of brain natriuretic peptide and markers of myocardial necrosis were measured on 1st , 2nd and 7th day after the onset of the first acute myocardial infarction, as well as after 3 and 6 months in 30 patients. Parameters of left ventricular remodeling were determined by echocardiographic investigation, which was performed in the acute phase and after 3 and 6 months.. Brain natriuretic peptide concentration was found to be related to the left ventricular geometry in the acute phase: brain natriuretic peptide peak level was lower in the patients with the normal left ventricular geometry than in the patients with the changed left ventricular geometry (140.6+/-63.3 pg/ml vs. 385.7+/-283.9, p<0.05). Brain natriuretic peptide concentration in the acute phase was higher in the patients who had increased left ventricular end diastolic diameter through 6-month period (348.9+/-309.4 pg/ml vs. 145.1+/-109.6 pg/ml, p<0.05). Higher troponin I (58.8+/-33.6 ng/ml vs. 30.9+/-31.3 ng/ml, p<0.05) and troponin T (4.5+/-2.2 ng/ml vs. 1.9+/-2.0 ng/ml, p<0.05) levels were also associated with left ventricular dilatation through 6 months after myocardial infarction.. Brain natriuretic peptide level in acute phase of myocardial infarction is related to the left ventricular geometry changes and remodeling. Brain natriuretic peptide together with other cardiac markers might be useful in predicting subsequent cardiac function. Topics: Aged; Biomarkers; Creatine Kinase, MB Form; Echocardiography; Female; Fluorescent Antibody Technique; Follow-Up Studies; Humans; Luminescence; Male; Middle Aged; Multivariate Analysis; Myocardial Infarction; Myoglobin; Natriuretic Peptide, Brain; Necrosis; Prognosis; Risk Factors; Time Factors; Troponin I; Ventricular Remodeling | 2004 |
N-terminal pro-brain natriuretic peptide in relation to inflammation, myocardial necrosis, and the effect of an invasive strategy in unstable coronary artery disease.
Topics: Biomarkers; Coronary Artery Disease; Humans; Interleukin-6; Myocarditis; Myocardium; Natriuretic Peptide, Brain; Necrosis; Nerve Tissue Proteins; Peptide Fragments; Troponin T | 2004 |
N-terminal pro-brain natriuretic peptide in relation to inflammation, myocardial necrosis, and the effect of an invasive strategy in unstable coronary artery disease.
We sought to examine whether measurements of N-terminal pro-brain natriuretic peptide (NT-proBNP), in addition to cardiac troponin T (cTnT) and interleukin-6 (IL-6), improve the ability to identify high-risk patients who benefit from an early invasive strategy.. Biochemical indicators of cardiac performance (e.g., NT-proBNP), inflammation (e.g., IL-6), and myocardial damage (e.g., cTnT) predict mortality in unstable coronary artery disease (UCAD) (i.e., unstable angina or non-ST-segment elevation myocardial infarction [MI]). In these patients, an early invasive treatment strategy improves the outcome.. Levels of NT-proBNP, cTnT, and IL-6 were measured in 2,019 patients with UCAD randomized to an invasive or non-invasive strategy in the FRagmin and fast revascularization during InStability in Coronary artery disease (FRISC-II) trial. Patients were followed up for two years to determine death and MI.. Patients in the third NT-proBNP tertile had a 4.1-fold (95% confidence interval [CI] 2.4 to 7.2) and 3.5-fold (95% CI 1.8 to 6.8) increased mortality in the non-invasive and invasive groups, respectively. An increased NT-proBNP level was independently associated with mortality. In patients with increased levels of both NT-proBNP and IL-6, an early invasive strategy reduced mortality by 7.3% (risk ratio 0.46, 95% CI 0.21 to 1.00). In patients with lower NT-proBNP or IL-6 levels, the mortality was not reduced. Only elevated cTnT was independently associated with future MI and a reduction of MI by means of an invasive strategy.. N-terminal proBNP is independently associated with mortality. The combination of NT-proBNP and IL-6 seems to be a useful tool in the identification of patients with a definite survival benefit from an early invasive strategy. Only cTnT is independently associated with future MI and a reduction of MI by an invasive strategy. Topics: Adult; Aged; Angina, Unstable; Biomarkers; Coronary Angiography; Coronary Disease; Echoencephalography; Humans; Inflammation; Interleukin-6; Male; Middle Aged; Myocardial Infarction; Natriuretic Peptide, Brain; Necrosis; Nerve Tissue Proteins; Peptide Fragments; Prognosis; Troponin T | 2003 |
Acute coronary syndromes--beyond myocyte necrosis.
Topics: Acute Disease; Angina, Unstable; Atrial Natriuretic Factor; Biomarkers; Coronary Artery Disease; Humans; Myocardial Infarction; Myocardium; Natriuretic Peptide, Brain; Necrosis; Pregnancy-Associated Plasma Protein-A; Prognosis; Risk Assessment | 2001 |